Composition having Anti-UVB damage function, skin care product, and use

Abstract

Disclosed are a composition having an anti-UVB damage function, a skin care product, and use, which can be used for solving the problem of UVB damage. The composition comprises: a first compound, wherein the first compound is selected from a compound represented by formula (I) or formula (II); formula (I):; formula (II):; and a second compound, wherein the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

Description

Compositions, skin care products and uses with anti-UVB damage function

[0001] Relevant publicly available cross-references

[0002] This disclosure claims priority to Chinese Patent Publication No. 2025100826058, filed on January 20, 2025, entitled "Composition with Anti-UVB Damage Function, Skin Care Product and Use", the entire contents of which are incorporated herein by reference. Technical Field

[0003] This disclosure relates to the field of anti-UVB damage technology, specifically to compositions, skin care products, and uses that have anti-UVB damage functions. Background Technology

[0004] UVB (ultraviolet radiation b) is a type of ultraviolet radiation, also known as medium-wave erythema-inducing ultraviolet radiation. UVB has an irritating effect on human skin, and excessive exposure to UVB can lead to skin cell damage.

[0005] Therefore, the problem of damage caused by UVB irradiation remains an unresolved issue.

[0006] Public content

[0007] One object of the embodiments of this disclosure is to solve at least one of the problems in the background described above and to provide corresponding beneficial effects.

[0008] Another object of the present disclosure is to provide a composition, skin care product and use having anti-UVB damage function, which can be used to solve the technical problem of anti-UVB damage.

[0009] The above objectives can be achieved mainly through the following technical solutions in the embodiments disclosed herein.

[0010] In one aspect, embodiments of this disclosure provide a composition comprising:

[0011] The first compound is selected from the compounds represented by formula (I) or formula (II);

[0012] Formula (I):

[0013] Equation (II): and

[0014] The second compound includes any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0015] In some alternative embodiments, the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0016] In some alternative embodiments, the first compound is the compound shown in formula (I), and the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (I) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or

[0017] The first compound is the compound shown in formula (I), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (I) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or

[0018] The first compound is the compound shown in formula (I), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (I) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or

[0019] The first compound is the compound shown in formula (I), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (I) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.5.

[0020] In some alternative embodiments, the first compound is the compound represented by formula (II); the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (II) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or

[0021] The first compound is the compound shown in formula (II), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (II) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or

[0022] The first compound is the compound shown in formula (II), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (II) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or

[0023] The first compound is the compound shown in formula (II), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (II) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.5.

[0024] In another aspect, embodiments of this disclosure provide the use of the above-described composition in the preparation of an anti-UVB damage formulation.

[0025] In another aspect, embodiments of this disclosure provide the use of the above-described composition in the preparation of a DNA damage inhibitor.

[0026] In another aspect, embodiments of this disclosure provide the use of the above-described composition in the preparation of an HMGB1 expression inhibitor.

[0027] In another aspect, embodiments of this disclosure provide the use of the above-described composition in the preparation of an SLC7A11 expression promoter.

[0028] In another aspect, embodiments of this disclosure provide a skincare product comprising:

[0029] The first compound, selected from compounds represented by formula (I) or formula (II); and

[0030] The second compound includes any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0031] In some alternative embodiments, the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0032] In some alternative embodiments, the first compound is the compound shown in formula (I), and the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (I) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or

[0033] The first compound is the compound shown in formula (I), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (I) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or

[0034] The first compound is the compound shown in formula (I), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (I) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or

[0035] The first compound is the compound shown in formula (I), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (I) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.5.

[0036] In some alternative embodiments, the first compound is the compound represented by formula (II); the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (II) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or

[0037] The first compound is the compound shown in formula (II), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (II) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or

[0038] The first compound is the compound shown in formula (II), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (II) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or

[0039] The first compound is the compound shown in formula (II), and the second compound is palmitoyl pentapeptide-4, with the mass ratio of the compound of formula (II) to palmitoyl pentapeptide-4 being 25:0.05 to 25:0.5.

[0040] The beneficial effects of this disclosure include:

[0041] In some embodiments, the compositions provided in this disclosure include a first compound and a second compound, which have the function of resisting UVB damage and can solve the problems in the background; for example, the composition can reduce the damage to skin cells caused by UVB irradiation through the synergistic effect of the combination of the first compound and the second compound, thereby achieving the effect of resisting UVB damage.

[0042] In some embodiments, the compositions provided in this disclosure can resist UVB damage through the synergistic effect of the first and second compounds, thereby protecting the skin.

[0043] In some embodiments, the compositions provided in this disclosure can protect the skin by resisting UVB damage and can be used to prevent or treat one or more skin diseases caused by UVB irradiation.

[0044] In some embodiments, when the first compound is selected from the compound shown in formula (I) and the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4, the composition provided in this disclosure can synergistically reduce the HMGB1 expression level of keratinocytes after UVB irradiation by the first and second compounds, thereby achieving anti-inflammatory effects.

[0045] In some embodiments, when the first compound is selected from the compound shown in formula (II) and the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4, the composition provided in this disclosure can synergistically increase the expression level of SLC7A11 in keratinocytes after UVB irradiation by the first and second compounds, thereby achieving anti-inflammatory effects.

[0046] In some embodiments, this disclosure provides the use of the above-described composition in the preparation of an anti-UVB damage formulation. Anti-UVB damage effects can be achieved by reducing HMGB1 or increasing SLC7A11 expression. Attached Figure Description

[0047] Figure 1 is an NMR diagram of the compound shown in formula (I) in an embodiment of this disclosure;

[0048] Figure 2 is a mass spectrum of the compound represented by formula (I) in the embodiments of this disclosure;

[0049] Figure 3 is an NMR diagram of the compound shown in formula (II) in an embodiment of this disclosure;

[0050] Figure 4 is a mass spectrum of the compound represented by formula (II) in the embodiments of this disclosure. Detailed Implementation

[0051] The present disclosure will now be described in further detail with reference to the accompanying drawings, so that those skilled in the art can implement it based on the description.

[0052] The terms "first," "second," etc., used in the embodiments of this disclosure are for descriptive purposes only and should not be construed as indicating or implying relative importance or implicitly specifying the number of indicated technical features. Therefore, a feature defined with "first," "second," etc., may explicitly or implicitly include at least one of that feature.

[0053] Furthermore, the terms “comprising,” “containing,” “having,” and any variations thereof are intended to cover non-exclusive inclusion. For example, a process, method, system, product, or apparatus that includes a series of steps or units is not limited to the steps or units listed, but may optionally include steps or units not listed, or may optionally include other steps or units inherent to such process, method, product, or apparatus.

[0054] In addition to the foregoing, it should be emphasized that the reference to "embodiment" herein means that a particular feature, structure, or characteristic described in connection with an embodiment may be included in at least one embodiment of this disclosure. The appearance of this phrase in various places throughout the specification does not necessarily refer to the same embodiment, nor is it a separate or alternative embodiment mutually exclusive with other embodiments. It will be explicitly and implicitly understood by those skilled in the art that the embodiments described herein can be combined with other embodiments.

[0055] <Composition>

[0056] In a first aspect, embodiments of this disclosure provide a composition comprising:

[0057] The first compound is selected from the compounds represented by formula (I) or formula (II);

[0058] Formula (I):

[0059] Equation (II): and

[0060] The second compound comprises any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4. In some optional embodiments, the second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0061] The composition of this disclosure includes a first compound and a second compound, which have the function of resisting UVB damage; the composition can reduce the damage to skin cells caused by UVB irradiation through the synergistic effect of the combination of the first compound and the second compound, thereby overcoming the defects in the prior art.

[0062] Furthermore, excessive UVB exposure can lead to inflammation of the skin. The composition of the first aspect embodiment reduces inflammation of skin cells (keratinocytes) caused by UVB irradiation by resisting UVB damage, thereby achieving an anti-inflammatory effect and further protecting the skin.

[0063] Furthermore, skin inflammation can even lead to various skin diseases. The composition of the first aspect embodiment described above can protect the skin by resisting UVB damage and can be used to prevent or treat one or more skin diseases caused by UVB irradiation.

[0064] In some alternative embodiments, the skin cells are keratinocytes (HaCaT for short).

[0065] Depending on the choice of the first compound and the second compound, the compositions of the embodiments of this disclosure may be selected from any one of the first composition to the eighth composition.

[0066] HMG1 (high mobility group 1 protein) was first extracted and identified from bovine thymus in 1973, named for its high migration ability in polyacrylamide gel electrophoresis. HMG can be further divided into three families: HMGA, HMGB, and HMGN. The HMGB family has three members: HMGB1, HMGB2, and HMGB3. HMGB1 (high mobility group 1 protein) is the most abundant HMG protein. Studies have shown that HMGB1 is a typical damage-associated molecular pattern (DAMP) signaling protein. When cells are subjected to DNA damage (such as radiation or chemical damage), HMGB1 is released extracellularly, becoming a common marker of necrotizing inflammation. UVB irradiation leads to high levels of HMGB1 expression.

[0067] In some alternative embodiments, when the composition is selected from any one of the first composition, the second composition, the third composition, and the fourth composition, the expression level of HMGB1 in keratinocytes increased by UVB irradiation can be reduced, the inflammatory response can be reduced, and the anti-UVB damage effect can be achieved.

[0068] In some optional embodiments, the composition is selected from the first composition, wherein the first compound is selected from the compound represented by formula (I), and the second compound is selected from palmitoyl tripeptide-5; the first compound and the second compound can synergistically reduce the HMGB1 expression level of keratinocytes increased by UVB irradiation, reduce the inflammatory response, and achieve the anti-UVB damage effect.

[0069] Optionally, the mass ratio of the compound of formula (I) to palmitoyl tripeptide-5 can be from 25:0.3 to 25:3.

[0070] For example, the mass ratio of the compound shown in formula (I) to palmitoyl tripeptide-5 can be 25:0.3, 25:0.4, 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, 25:2.1, 25:2.2, 25:2.3, 25:2.4, 25:2.5, 25:2.6, 25:2.7, 25:2.8, 25:2.9, or 25:3, etc.

[0071] In some optional embodiments, the composition is selected from the second composition, wherein the first compound is selected from the compound shown in formula (I), and the second compound is selected from acetyl dipeptide-1 cetyl ester; the first compound and the second compound can synergistically reduce the HMGB1 expression level of keratinocytes increased by UVB irradiation, reduce the inflammatory response, and achieve the anti-UVB damage effect.

[0072] Optionally, the mass ratio of the compound of formula (I) to acetyl dipeptide-1 cetyl ester can be from 25:0.5 to 25:4.

[0073] For example, the mass ratio of compound (I) to acetyl dipeptide-1 cetyl ester can be 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, or 25:1.8. :2.1 or 25:2.2 or 25:2.3 or 25:2.4 or 25:2.5 or 25:2.6 or 25:2.7 or 25:2.8 or 25:2.9 or 25:3 or 25:3.1 or 25:3.2 or 25:3.3 or 25:3.4 or 25:3.5 or 25:3.6 or 25:3.7 or 25:3.8 or 25:3.9 or 25:4 etc.

[0074] In some optional embodiments, the composition is selected from the third composition, wherein the first compound is selected from the compound represented by formula (I), and the second compound is selected from acetyl tripeptide-30 citrulline; the first and second compounds can synergistically reduce the HMGB1 expression level of keratinocytes increased by UVB irradiation, reduce the inflammatory response, and achieve the anti-UVB damage effect.

[0075] Optionally, the mass ratio of the compound of formula (I) to acetyl tripeptide-30 citrulline can be from 25:0.5 to 25:3.

[0076] For example, the mass ratio of compound (I) to acetyl tripeptide-30 citrulline can be 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, 25:2.1, 25:2.2, 25:2.3, 25:2.4, 25:2.5, 25:2.6, 25:2.7, 25:2.8, 25:2.9, or 25:3, etc.

[0077] In some optional embodiments, the composition is selected from the fourth composition, wherein the first compound is selected from the compound represented by formula (I), and the second compound is selected from palmitoyl pentapeptide-4; the first and second compounds can synergistically reduce the HMGB1 expression level of keratinocytes increased by UVB irradiation, reduce the inflammatory response, and achieve the anti-UVB damage effect.

[0078] Optionally, the mass ratio of the compound of formula (I) to palmitoyl pentapeptide-4 can be from 25:0.05 to 25:0.5.

[0079] For example, the mass ratio of compound (I) to palmitoyl pentapeptide-4 can be 25:0.05, 25:0.1, 25:0.15, 25:0.2, 25:0.25, 25:0.3, 25:0.35, 25:0.4, 25:0.45, or 25:0.5, etc.

[0080] SLC7A11 (Solute Carrier Family 7 Member 11) is a cysteine ​​transporter with high specificity for cysteine ​​and glutamate. Its function is to participate in the extracellular uptake of cysteine ​​and the release of glutamate, promote glutathione synthesis, protect cells from oxidative stress damage, maintain cellular redox balance, and thus prevent cell death caused by lipid peroxidation. UVB irradiation leads to a decrease in the expression level of SLC7A11.

[0081] In some alternative embodiments, when the composition is selected from any one of the fifth, sixth, seventh, and eighth compositions, it can increase the SLC7A11 expression level in keratinocytes that is reduced by UVB irradiation, reduce the inflammatory response, and achieve an anti-UVB damage effect.

[0082] In some optional embodiments, the composition is selected from the fifth composition, wherein the first compound is selected from the compound represented by formula (II) and the second compound is selected from palmitoyl tripeptide-5; the first and second compounds can synergistically increase the SLC7A11 expression level of keratinocytes that decreases due to UVB irradiation, reduce the inflammatory response, and achieve the anti-UVB damage effect.

[0083] Optionally, the mass ratio of the compound of formula (II) to palmitoyl tripeptide-5 can be from 25:0.3 to 25:3.

[0084] For example, the mass ratio of compound (II) to palmitoyl tripeptide-5 can be 25:0.3, 25:0.4, 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, 25:2.1, 25:2.2, 25:2.3, 25:2.4, 25:2.5, 25:2.6, 25:2.7, 25:2.8, 25:2.9, or 25:3, etc.

[0085] In some optional embodiments, the composition is selected from the sixth composition, wherein the first compound is selected from the compound represented by formula (II) and the second compound is selected from acetyl dipeptide-1 cetyl ester; the first and second compounds can synergistically increase the SLC7A11 expression level of keratinocytes that decreases due to UVB irradiation, reduce the inflammatory response, and achieve the effect of anti-UVB damage.

[0086] Optionally, the mass ratio of the compound of formula (II) to acetyl dipeptide-1 cetyl ester can be from 25:0.5 to 25:4.

[0087] For example, the mass ratio of compound (II) to acetyl dipeptide-1 cetyl ester can be 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, or 2... 5:2.1 or 25:2.2 or 25:2.3 or 25:2.4 or 25:2.5 or 25:2.6 or 25:2.7 or 25:2.8 or 25:2.9 or 25:3 or 25:3.1 or 25:3.2 or 25:3.3 or 25:3.4 or 25:3.5 or 25:3.6 or 25:3.7 or 25:3.8 or 25:3.9 or 25:4 etc.

[0088] In some optional embodiments, the composition is selected from the seventh composition, wherein the first compound is selected from the compound represented by formula (II), and the second compound is selected from acetyl tripeptide-30 citrulline; the first and second compounds can synergistically increase the SLC7A11 expression level of keratinocytes that decreases due to UVB irradiation, reduce the inflammatory response, and achieve the effect of anti-UVB damage.

[0089] Optionally, the mass ratio of the compound of formula (II) to acetyl tripeptide-30 citrulline can be from 25:0.5 to 25:3.

[0090] For example, the mass ratio of compound (II) to acetyl tripeptide-30 citrulline can be 25:0.5, 25:0.6, 25:0.7, 25:0.8, 25:0.9, 25:1, 25:1.1, 25:1.2, 25:1.3, 25:1.4, 25:1.5, 25:1.6, 25:1.7, 25:1.8, 25:1.9, 25:2, 25:2.1, 25:2.2, 25:2.3, 25:2.4, 25:2.5, 25:2.6, 25:2.7, 25:2.8, 25:2.9, or 25:3, etc.

[0091] In some optional embodiments, the composition is selected from the eighth composition, wherein the first compound is selected from the compound represented by formula (II) and the second compound is selected from palmitoyl pentapeptide-4; the first and second compounds can synergistically increase the SLC7A11 expression level of keratinocytes that decreases due to UVB irradiation, reduce the inflammatory response, and achieve the effect of anti-UVB damage.

[0092] Optionally, the mass ratio of the compound of formula (II) to palmitoyl pentapeptide-4 can be from 25:0.05 to 25:0.5.

[0093] For example, the mass ratio of compound (II) to palmitoyl pentapeptide-4 can be 25:0.05, 25:0.1, 25:0.15, 25:0.2, 25:0.25, 25:0.3, 25:0.35, 25:0.4, 25:0.45, or 25:0.5, etc.

[0094] The aforementioned palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 can be obtained by direct purchase or synthesized by methods known to those skilled in the art.

[0095] In some alternative embodiments, the above composition is a skin care composition that can be used for skin care.

[0096] In some optional embodiments, the above composition may be in the form of creams, ointments, creams, honey, fats, lotions, milk, milk liquids, etc.; or in the form of liquids such as dew, liquid, water, oil, oil-water separation, etc.; or in the form of gels such as gels, glues, etc.; or in the form of powders such as loose powders, granules, etc.; or in the form of block powders, large solid blocks, etc.; or in the form of mud-like solids; or in the form of wax-based materials with wax as the main base; or in the form of freeze-dried powders, freeze-dried tablets, etc.; or in the form of propellant-free sprays, etc.; or in the form of propellant-containing aerosols, etc.; or in the form of patches, films, etc. containing substrates for use in conjunction with cosmetics.

[0097] In some alternative embodiments, the above composition may be applied topically to hair, body hair, torso, head, face, eyes, lips, hands, feet, whole body skin, fingers (toes), and nails.

[0098] In some alternative embodiments, the above composition may contain at least one cosmetically acceptable adjuvant. The adjuvant is selected from one or more of surfactants and / or emulsifiers, preservatives, buffers, chelating agents, denaturants, opacifiers, pH adjusters, reducing agents and stabilizers, thickeners, gelling agents, film-forming polymers, fillers, matting agents, gloss agents, pigments, dyes, fragrances, and mixtures thereof.

[0099] In some optional embodiments, the above composition may contain at least one cosmetically acceptable active ingredient selected from caffeine, caffeic acid, cyclic peptides, vitamin A and its derivatives, retinol, vitamin C and its derivatives, vitamin E and its derivatives, arbutin, cinnamic acid and its derivatives, ferulic acid, ergothioneine, tetrahydromethylpyrimidine carboxylic acid, glycyrrhizin, bisabolol, ceramides, phenylethyl resorcinol, soluble collagen, adenosine, 4-butylresorcinol, hydrolyzed collagen, inositol, saccharide isomers, fibronectin, astaxanthin, asiaticoside, rhamnose, resveratrol, amino acids, hydroxypropyltetrahydropyrantriol, fermentation products, sodium hyaluronate, nicotinamide, panthenol, and plant extracts, or one or more of these.

[0100] In some optional embodiments, the above composition may further include a solvent, which may be selected from one or more of dibutyl bis(2-ethylhexanoate), isononyl isononyl ester, pentaerythritol tetra(ethylhexanoate), caprylic / decanoic acid triglyceride, cetyl ethylhexanoate, diisostearyl malate, and octyl dodecyl alcohol.

[0101] In some alternative embodiments, the above composition may also include cosmetically acceptable adjuvants.

[0102] In some optional embodiments, the mass concentration (mass fraction) of the first and second compounds can be 0.0001% to 10% of the total weight of the composition.

[0103] The compound of formula (I) above can be obtained by direct purchase or by synthesis using the methods shown in steps S11 to S13:

[0104] Step S11: In a 50 mL round-bottom flask, add 466 mg of ferulic acid (3-methoxy-4-hydroxycinnamic acid), dissolve in 10 mL of dichloromethane, then add 1.4 mL of triethylamine. Stir the resulting reaction solution magnetically and cool it to 0–5 °C in an ice-water bath. Slowly add 900 mg of tert-butyldimethylchlorosilane and stir at room temperature for 4 hours. After the reaction is complete, add 25 mL of ice water to quench the reaction. Extract the aqueous layer with dichloromethane (25 mL × 3), combine the organic layers, dry the organic layer with anhydrous sodium sulfate, filter, and concentrate under vacuum to obtain the crude product. Dissolve the crude product in 20 mL of tetrahydrofuran and 2 mL of water, add 200 mg of anhydrous potassium carbonate, and stir at room temperature for 6 hours. After the reaction is complete, add 25 mL of water and extract the aqueous layer with ethyl acetate (25 mL × 3), combine the organic layers, concentrate under vacuum, and recrystallize with petroleum ether to obtain the first intermediate.

[0105] Step S12: In a 50 mL brown round-bottom flask, add 308 mg of the first intermediate, 343 mg of retinol, 288 mg of EDCI, and 12 mg of DMAP. Dissolve the residue in 5 mL of tetrahydrofuran, and finally add 270 μL of TEA. Stir the mixture at room temperature for 12 hours. After the reaction is complete, concentrate the reaction solution under vacuum, add 25 mL of water, and extract the aqueous layer with ethyl acetate (25 mL × 3). Combine the organic layers, dry the organic layer with anhydrous sodium sulfate, filter, and concentrate under vacuum to obtain the crude product. Use silica gel column chromatography (petroleum ether:ethyl acetate = 20:1 as eluent) to obtain the second intermediate.

[0106] Step S13: Add 384 mg of the second intermediate to a 50 mL brown round-bottom flask, dissolve in 8 mL of tetrahydrofuran, cool to 0 °C–5 °C in an ice-water bath, slowly add 600 μL of tetrabutylammonium fluoride, and stir in an ice bath for 10 minutes. Concentrate under vacuum to obtain the crude product, and obtain compound (I) by silica gel column chromatography (petroleum ether:ethyl acetate = 5:1 as eluent).

[0107] The mass spectrometry data of compound (I) are shown in Figure 2.

[0108] The NMR spectra of the compound of formula (I) are shown in Figure 1, and the data are as follows:

[0109] 1 H NMR (500MHz, CDCl3) δ7.62(d,J=15.9Hz,1H),7.07(dd,J=8.3,2.0Hz,1H),7.02(d,J=1.9Hz,1H ),6.91(d,J=8.2Hz,1H),6.65(dd,J=15.1,11.2Hz,1H),6.30(d,J=15.9Hz,2H),6.22-6.06(m, 3H),5.90(s,1H),5.69(t,J=7.2Hz,1H),4.86(d,J=7.2Hz,2H),3.92(s,3H),2.01(t,J=6.3Hz, 2H),1.96(s,3H),1.93(s,3H),1.71(s,3H),1.63-1.57(m,2H),1.49-1.44(m,2H),1.02(s,6H).

[0110] Compound (II) can be obtained by direct purchase or by synthesis using the methods shown in steps S21 to S27:

[0111] Step S21: Mix 3-(benzo[d][1,3]dioxapentane-5-yl)acrylic acid, psoralen, 1-ethyl-(3-dimethylaminopropyl)carbodiimide hydrochloride, 4-dimethylaminopyridine, triethylamine and tetrahydrofuran and stir evenly at room temperature to obtain a mixture.

[0112] In practice, 4.5 g (22.6 mmol, 1.5 equiv) of 3-(benzo[d][1,3]dioxapentane-5-yl)acrylic acid, 4.5 g (15 mmol, 1 equiv) of psoralen, 5.76 g (30 mmol, 2 equiv) of 1-ethyl-(3-dimethylaminopropyl)carbodiimide hydrochloride, 180 mg (1.5 mmol, 0.1 equiv) of 4-dimethylaminopyridine, 4.8 mL (37.6 mmol, 2.5 equiv) of triethylamine, and 80 mL of tetrahydrofuran can be added to a 200 mL reactor and stirred at room temperature for 12 hours to obtain a mixture.

[0113] Step S22: The mixture above is subjected to a first vacuum concentration to obtain a first concentrate.

[0114] The mixture was concentrated under reduced pressure at a temperature of 40±5℃ to obtain the first concentrate.

[0115] Step S23: Extract the target layer from the first concentrate dissolved in water with ethyl acetate and collect the organic layer.

[0116] In practice, firstly, 200 mL of water is added to the first concentrate to dissolve it. Then, the aqueous layer of the first concentrate after water dissolution is extracted with ethyl acetate (200 mL × 3) to a target number of extractions. The target number of extractions is ≥1. Finally, the organic layers are combined.

[0117] Step S24: Perform a second vacuum concentration on the dried organic layer to obtain a second concentrate.

[0118] In practice, firstly, 10g of anhydrous sodium sulfate is added to the organic layer to dry it and then filter it to obtain the dried organic layer. Then, the dried organic layer is concentrated under reduced pressure at 40±5℃ to obtain a second concentrate (oily crude product).

[0119] Step S25: Add petroleum ether to the second concentrate and perform a third vacuum concentration to obtain the first solid.

[0120] In practice, 60 mL of petroleum ether is added to the second concentrate and the mixture is concentrated under reduced pressure at a temperature of 40±5℃ to obtain the first solid (yellow solid).

[0121] Step S26: Mix the mixture with the first solid and then pulverize and filter to obtain a filter cake.

[0122] The mixture comprises petroleum ether and ethyl acetate, wherein the volume ratio of petroleum ether to ethyl acetate is 50:1.

[0123] In practice, a mixture of 200 mL of petroleum ether and ethyl acetate is mixed with the first solid and stirred for 30 minutes, then filtered through a Buchner funnel to obtain a filter cake.

[0124] Step S27: Vacuum dry the above filter cake to obtain compound (II).

[0125] In practice, the filter cake was vacuum dried at a temperature of 40±5℃ to obtain compound (II). Specifically, the mass spectrum of compound (II) is shown in Figure 4.

[0126] The NMR spectra of compound (II) are shown in Figure 3, and the data are as follows:

[0127] 1 H NMR (500MHz, CDCl3) δ7.77(d,J=15.9Hz,1H),7.39(d,J=8.6Hz,2H),7.10(d,J=2.0Hz,1H),7.09(q,J=2 .8,2.3Hz,2H),7.06(dd,J=8.1,1.7Hz,1H),6.84(d,J=8.0Hz,1H),6.44(d,J=15.9Hz,1H),6.32(d,J=16 .2Hz,1H),6.18(d,J=16.3Hz,1H),6.03(s,2H),5.89(dd,J=17.5,10.7Hz,1H),5.11(tt,J=7.1,1.4Hz,1 H),5.08-4.99(m,2H),1.96(q,J=7.5Hz,2H),1.68(s,3H),1.59(s,3H),1.54-1.48(m,2H),1.21(s,3H).

[0128] The nuclear magnetic resonance (NMR) data were obtained using an NMR spectrometer (model: AVANCE III HD 400MHz, manufacturer: Bruker, Switzerland).

[0129] In some embodiments, the wavelength of UVB is 320 nm to 400 nm.

[0130] <Skincare Products>

[0131] As can be seen from the foregoing, the composition provided in the first aspect embodiment can reduce the inflammatory response in skin cells caused by UVB irradiation and has a skin care effect. In some embodiments, the composition can be used as a skin care product or further used to prepare a skin care product.

[0132] According to the composition provided in the first aspect embodiment, this disclosure embodiment can also provide a skin care product, the skin care product comprising:

[0133] The first compound, selected from compounds represented by formula (I) or formula (II); and

[0134] The second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

[0135] The skincare product provided in this disclosure includes a first compound and a second compound, which have a UVB damage-inducing effect. Through the synergistic effect of the combination of the first and second compounds, the inflammatory response of skin cells (keratinocytes) caused by UVB irradiation can be reduced, achieving an anti-inflammatory effect.

[0136] In some embodiments, the skin care product may also include a solvent, which is a cosmetically acceptable solvent, such as one or more of dibutyl bis(2-ethylhexanoate), isononyl bis(2-ethylhexanoate), pentaerythritol tetra(ethylhexanoate), caprylic / capric triglyceride, cetyl ethylhexanoate, diisostearyl malate, and octyl dodecyl alcohol.

[0137] In some optional embodiments, the sum of the concentrations of the first compound, the second compound, and the solvent is 0.0001% to 10% of the total weight of the skin care product.

[0138] In some alternative embodiments, the skincare product includes: a cosmetically acceptable adjuvant.

[0139] <Applications>

[0140] In some optional embodiments, this disclosure provides the use of the composition with anti-UVB damage function provided in the first aspect in the preparation of skin care products. Anti-UVB damage can be achieved by reducing the expression of HMGB1 or increasing the expression of SLC7A11, thus achieving a skin care effect.

[0141] In some optional embodiments, this disclosure provides the use of the composition provided in the first aspect in the preparation of an anti-UVB damage formulation. The anti-UVB damage effect can be achieved by reducing HMGB1 or increasing SLC7A11 expression.

[0142] In some optional embodiments, this disclosure provides the use of the composition provided in the first aspect in the preparation of a DNA damage inhibitor. By reducing the expression of HMGB1 or increasing the expression of SLC7A11, it can resist DNA damage, thereby achieving an anti-UVB damage effect.

[0143] In some optional embodiments, this disclosure provides the use of the composition provided in a first aspect in the preparation of an HMGB1 expression inhibitor, wherein the composition is selected from any one of a first composition, a second composition, a third composition, and a fourth composition. By reducing the expression of HMGB1, an anti-UVB damage effect can be achieved.

[0144] In some optional embodiments, this disclosure provides the use of the composition provided in the first aspect in the preparation of an SLC7A11 expression promoter, wherein the composition is selected from any one of the fifth, sixth, seventh, and eighth compositions. By increasing the expression of SLC7A11, an anti-UVB damage effect can be achieved.

[0145] <Experiment>

[0146] experimental cells

[0147] Keratinocytes HaCaT

[0148] Experimental reagents

[0149] Compound of formula (I).

[0150] Compound of formula (II).

[0151] Palmitoyl tripeptide-5 (from Genscript Biotech Inc.)

[0152] Acetyl dipeptide-1 cetyl ester (from Genscript Biotech Inc.)

[0153] Acetyl tripeptide-30 citrulline (from Genscript Biotech Inc.)

[0154] Palmitoyl pentapeptide-4 (from Genscript Biotech Inc.)

[0155] DMEM (dulbecco's modified eagle medium): This is a basic culture medium purchased from Gibco biological medium of Thermo Fisher Scientific (China) Co., Ltd., product code C11995500BT.

[0156] Fetal bovine serum (FBS): Gibco brand fetal bovine serum purchased from Thermo Fisher Scientific (China) Co., Ltd., product code 10091148.

[0157] Penicillin / Streptomycin: Gibco brand penicillin / streptomycin, catalog number 25200114, purchased from Thermo Fisher Scientific (China) Co., Ltd., is a penicillin / streptomycin solution (10,000 U / mL), which includes penicillin and streptomycin at concentrations of 10,000 U / mL.

[0158] Phosphate-buffered saline (PBS): pH 7.4, is a balanced salt solution suitable for various cell culture applications, such as washing cells before dissociation, transporting cells or tissues, diluting cells for counting, and preparing reagents; purchased from Thermo Fisher Scientific (China) Co., Ltd.

[0159] An RNA extraction kit, specifically the TransZol Up Plus RNA Kit (Transgen Biotech), purchased from Beijing TransGen Biotech Co., Ltd., is suitable for extracting total RNA from cells and tissues. The sample is lysed using TransZol Up, and after adding the RNA Extraction Agent, the solution separates into a colorless aqueous phase and a pink organic phase, with RNA in the aqueous phase. The RNA in the aqueous phase is then specifically adsorbed using a silica gel membrane centrifuge column. The RNA extraction kit specifically includes the following components: TransZol Up 100ml, RNA Extraction Agent 20ml, Clean Buffer 9 (CB9) 110ml, Wash Buffer 9 (WB9) 24ml, RNase-free Water 40ml, RNase-free Tube (1.5ml) 100each, and RNA Spin Columns with Collection Tubes 100each.

[0160] Using an M-MLV reverse transcriptase reverse transcription kit, the Evo M-MLV Reverse Transcription Premix Kit (with gDNA removal reagent for qPCR) Ver.2 (Agbio, AG11728) was selected. This kit contains 5X Evo M-MLV RT Reaction Mix, and the cDNA product can be directly used for qPCR detection. The Evo M-MLV Reverse Transcription Premix Kit (with gDNA removal reagent for qPCR) Ver.2 contains all the components required for the reverse transcription reaction.

[0161] The premixed solution for 2× real-time quantitative PCR amplification (English name: 2×qPCR SYBR Green Master Mix, abbreviated as SYBR Mix) contains hot-start DNA polymerase. DNA Polymerase), SYBR Green I, deoxyribonucleoside triphosphates (dNTPs), magnesium ions (Mg) 2+ ) qPCR SYBR Green Master Mix can be selected in specific ways. qPCR SYBR Green Master Mix (No Rox) is available from Yeasen under product number 11202ES.

[0162] Experimental equipment

[0163] CO2 incubator (Thermo, 150I).

[0164] Clean bench (Su Jing An Tai, SW-CJ-1F).

[0165] Micro-volume spectrophotometer (Thermo Scientific NanoDrop).

[0166] ProFlex TM PCR instrument (Applied Biosystems SimpliAmp PCR thermal cycler).

[0167] QPCR instrument (Applied Biosystems QuantStudio 1).

[0168] UVB crosslinker (Luyor UCL-3500).

[0169] High-speed refrigerated centrifuge (Eppendorf Centrifuge 5418R).

[0170] Experimental samples and preparation:

[0171] 1. Relevant solutions used for sample preparation

[0172] The basal culture medium solution is a DMEM culture medium solution containing FBS and penicillin / streptomycin, specifically a DMEM culture medium solution containing 10% FBS and 1% penicillin / streptomycin; wherein the mass fraction of FBS is 10% and the mass fraction of penicillin / streptomycin is 1%; this basal culture medium solution can be prepared by mixing FBS, penicillin / streptomycin and DMEM culture medium.

[0173] Mother liquor containing compound (I): Mix compound (I) powder into dimethyl sulfoxide (DMSO) to form mother liquor, the concentration of which can be adjusted as needed.

[0174] Mother liquor containing compound (II): Mix compound (II) powder into DMSO to form mother liquor, the concentration of which can be adjusted as needed.

[0175] Palmitoyl tripeptide-5 stock solution: Palmitoyl tripeptide-5 powder is mixed into DMSO to form palmitoyl tripeptide-5 stock solution, and the concentration can be adjusted as needed.

[0176] Palmitoyl tripeptide-5 stock solution: Acetyl dipeptide-1 powder is mixed into DMSO to form palmitoyl tripeptide-5 stock solution. The concentration can be adjusted as needed.

[0177] Acetyl tripeptide-30 citrulline stock solution: Acetyl tripeptide-30 citrulline powder is mixed into water to form acetyl tripeptide-30 citrulline stock solution. The concentration can be adjusted as needed.

[0178] Palmitoyl pentapeptide-4 stock solution: Palmitoyl pentapeptide-4 powder is mixed into DMSO to form palmitoyl pentapeptide-4 stock solution. The concentration can be adjusted as needed.

[0179] 2. Sample

[0180] Blank control group sample: Basal culture medium solution was selected as the blank control group sample.

[0181] UVB control group sample: The basal culture medium solution was selected as the UVB control group sample.

[0182] Sample 1-1: A DMEM culture medium solution containing compound (I) at a concentration of 12.5 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (I) with basal culture medium solution to a concentration of compound (I) of 12.5 μg / mL.

[0183] Sample 1-2: DMEM medium solution containing palmitoyl tripeptide-5 at a concentration of 0.15 μg / mL. Specifically, the palmitoyl tripeptide-5 stock solution was diluted with basal medium solution to a concentration of 0.15 μg / mL to obtain the sample.

[0184] Samples 1-3: DMEM medium solutions containing palmitoyl tripeptide-5 at a concentration of 1.5 μg / mL. Specifically, the palmitoyl tripeptide-5 stock solution was diluted with basal medium solution to a concentration of 12.5 μg / mL to obtain the sample.

[0185] Samples 1-4: DMEM medium solutions containing compound (I) at a concentration of 12.5 μg / mL and palmitoyl tripeptide-5 at a concentration of 0.15 μg / mL. Specifically, the samples were diluted by mixing the basal medium solution with the stock solution containing compound (I) and the stock solution containing palmitoyl tripeptide-5 until the concentration of compound (I) was 12.5 μg / mL and the concentration of palmitoyl tripeptide-5 was 0.15 μg / mL.

[0186] Samples 1-5: DMEM medium solutions containing compound (I) at a concentration of 12.5 μg / mL and palmitoyl tripeptide-5 at a concentration of 1.5 μg / mL. Specifically, the samples were diluted by mixing the basal medium solution with the stock solution containing compound (I) and the stock solution containing palmitoyl tripeptide-5 until the concentration of compound (I) was 12.5 μg / mL and the concentration of palmitoyl tripeptide-5 was 1.5 μg / mL.

[0187] Sample 2-1: A DMEM culture medium solution containing compound (I) at a concentration of 12.5 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (I) with basal culture medium solution to a concentration of compound (I) of 12.5 μg / mL.

[0188] Sample 2-2: A DMEM medium solution containing acetyl dipeptide-1 cetyl ester at a concentration of 0.25 μg / mL. Specifically, the acetyl dipeptide-1 cetyl ester stock solution was diluted with basal medium solution to a concentration of acetyl dipeptide-1 cetyl ester of 0.25 μg / mL to obtain this sample.

[0189] Sample 2-3: DMEM medium solution containing acetyl dipeptide-1 cetyl ester at a concentration of 2.0 μg / mL. Specifically, the acetyl dipeptide-1 cetyl ester stock solution was diluted with basal medium solution to a concentration of acetyl dipeptide-1 cetyl ester of 2.0 μg / mL to obtain the sample.

[0190] Samples 2-4: DMEM culture medium solutions containing compound (I) at a concentration of 12.5 μg / mL and acetyl dipeptide-1 cetyl ester at a concentration of 0.25 μg / mL. Specifically, the samples were diluted by mixing the basal culture medium solution with the stock solution containing compound (I) and the stock solution containing acetyl dipeptide-1 cetyl ester until the concentration of compound (I) was 12.5 μg / mL and the concentration of acetyl dipeptide-1 cetyl ester was 0.25 μg / mL.

[0191] Samples 2-5: DMEM culture medium solutions containing compound (I) at a concentration of 12.5 μg / mL and acetyl dipeptide-1 cetyl ester at a concentration of 2.0 μg / mL. Specifically, the samples were diluted by mixing the basal culture medium solution with the stock solution containing compound (I) and acetyl dipeptide-1 cetyl ester stock solution until the concentration of compound (I) was 12.5 μg / mL and the concentration of acetyl dipeptide-1 cetyl ester was 2.0 μg / mL.

[0192] Sample 3-1: A DMEM culture medium solution containing compound (I) at a concentration of 12.5 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (I) with basal culture medium solution to a concentration of compound (I) of 12.5 μg / mL.

[0193] Sample 3-2: A DMEM medium solution containing acetyl tripeptide-30 citrulline at a concentration of 0.25 μg / mL. Specifically, the acetyl tripeptide-30 citrulline stock solution was diluted with basal medium solution to a concentration of 0.15 μg / mL to obtain the sample.

[0194] Sample 3-3: A DMEM medium solution containing acetyl tripeptide-30 citrulline at a concentration of 1.5 μg / mL. Specifically, the acetyl tripeptide-30 citrulline stock solution was diluted with basal medium solution to a concentration of 1.5 μg / mL to obtain the sample.

[0195] Sample 3-4: DMEM medium solution containing compound (I) at a concentration of 12.5 μg / mL and acetyl tripeptide-30 citrulline at a concentration of 0.15 μg / mL. Specifically, the sample was diluted by mixing the basal medium solution with the stock solution containing compound (I) and the stock solution containing acetyl tripeptide-30 citrulline until the concentration of compound (I) was 12.5 μg / mL and the concentration of acetyl tripeptide-30 citrulline was 0.25 μg / mL.

[0196] Samples 3-5: DMEM culture medium solutions containing compound (I) at a concentration of 12.5 μg / mL and acetyl tripeptide-30 citrulline at a concentration of 1.5 μg / mL. Specifically, the basal culture medium solution and the stock solution containing compound (I) and acetyl tripeptide-30 citrulline were mixed and diluted to a concentration of 12.5 μg / mL for compound (I) and 1.5 μg / mL for acetyl tripeptide-30 citrulline to obtain the sample.

[0197] Sample 4-1: A DMEM culture medium solution containing compound (I) at a concentration of 12.5 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (I) with basal culture medium solution to a concentration of compound (I) of 12.5 μg / mL.

[0198] Sample 4-2: A DMEM medium solution containing palmitoyl pentapeptide-4 at a concentration of 0.025 μg / mL. Specifically, the sample is obtained by diluting the palmitoyl pentapeptide-4 stock solution with basal medium solution to a concentration of 0.025 μg / mL.

[0199] Sample 4-3: A DMEM medium solution containing palmitoyl pentapeptide-4 at a concentration of 0.25 μg / mL. Specifically, the palmitoyl pentapeptide-4 stock solution was diluted with basal medium solution to a concentration of 0.25 μg / mL to obtain this sample.

[0200] Sample 4-4: A DMEM medium solution containing compound (I) at a concentration of 12.5 μg / mL and palmitoyl pentapeptide-4 at a concentration of 0.025 μg / mL. Specifically, the sample was diluted by mixing the basal medium solution with the stock solution containing compound (I) and the stock solution containing acetyl tripeptide-30 citrulline until the concentration of compound (I) was 12.5 μg / mL and the concentration of palmitoyl pentapeptide-4 was 0.025 μg / mL.

[0201] Samples 4-5: DMEM medium solution containing compound (I) at a concentration of 12.5 μg / mL and palmitoyl pentapeptide-4 at a concentration of 0.25 μg / mL. Specifically, the sample was diluted by mixing the basal medium solution with the stock solution containing compound (I) and the stock solution containing acetyl tripeptide-30 citrulline until the concentration of compound (I) was 12.5 μg / mL and the concentration of palmitoyl pentapeptide-4 was 0.25 μg / mL.

[0202] Sample 5-1: A DMEM culture medium solution containing compound (II) at a concentration of 150 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (II) with basal culture medium solution to a concentration of compound (II) of 150 μg / mL.

[0203] Sample 5-2: A DMEM medium solution containing palmitoyl tripeptide-5 at a concentration of 1.8 μg / mL. Specifically, the palmitoyl tripeptide-5 stock solution was diluted with basal medium solution to a concentration of 1.8 μg / mL to obtain the sample.

[0204] Sample 5-3: A DMEM medium solution containing palmitoyl tripeptide-5 at a concentration of 18 μg / mL. Specifically, the palmitoyl tripeptide-5 stock solution was diluted with basal medium solution to a concentration of 18 μg / mL to obtain this sample.

[0205] Sample 5-4: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and palmitoyl tripeptide-5 at a concentration of 1.8 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and the stock solution containing palmitoyl tripeptide-5 to dilute the solution to a concentration of 150 μg / mL for compound (II) and a concentration of 1.8 μg / mL for palmitoyl tripeptide-5.

[0206] Sample 5-5: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and palmitoyl tripeptide-5 at a concentration of 18 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and the stock solution containing palmitoyl tripeptide-5 to dilute the solution to a concentration of 150 μg / mL for compound (II) and 18 μg / mL for palmitoyl tripeptide-5.

[0207] Sample 6-1: A DMEM culture medium solution containing compound (II) at a concentration of 150 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (II) with basal culture medium solution to a concentration of compound (II) of 150 μg / mL.

[0208] Sample 6-2: A DMEM medium solution containing acetyl dipeptide-1 cetyl ester at a concentration of 3 μg / mL. Specifically, the acetyl dipeptide-1 cetyl ester stock solution was diluted with basal medium solution to a concentration of 3 μg / mL to obtain the sample.

[0209] Sample 6-3: A DMEM medium solution containing acetyl dipeptide-1 cetyl ester at a concentration of 24 μg / mL. Specifically, the acetyl dipeptide-1 cetyl ester stock solution was diluted with basal medium solution to a concentration of 24 μg / mL to obtain this sample.

[0210] Sample 6-4: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and acetyl dipeptide-1 cetyl ester at a concentration of 3 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and acetyl dipeptide-1 cetyl ester to dilute the solution until the concentration of compound (II) was 150 μg / mL and the concentration of acetyl dipeptide-1 cetyl ester was 3 μg / mL.

[0211] Sample 6-5: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and acetyl dipeptide-1 cetyl ester at a concentration of 24 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and acetyl dipeptide-1 cetyl ester to dilute the solution until the concentration of compound (II) was 150 μg / mL and the concentration of acetyl dipeptide-1 cetyl ester was 24 μg / mL.

[0212] Sample 7-1: A DMEM culture medium solution containing compound (II) at a concentration of 150 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (II) with basal culture medium solution to a concentration of compound (II) of 150 μg / mL.

[0213] Sample 7-2: A DMEM medium solution containing acetyl tripeptide-30 citrulline at a concentration of 3 μg / mL. Specifically, the acetyl tripeptide-30 citrulline stock solution was diluted with basal medium solution to a concentration of 3 μg / mL to obtain the sample.

[0214] Sample 7-3: A DMEM medium solution containing acetyl tripeptide-30 citrulline at a concentration of 18 μg / mL. Specifically, the acetyl tripeptide-30 citrulline stock solution was diluted with basal medium solution to a concentration of 18 μg / mL to obtain the sample.

[0215] Sample 7-4: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and acetyl tripeptide-30 citrulline at a concentration of 3 μg / mL. Specifically, the sample is obtained by mixing the basal medium solution with the stock solution containing compound (II) and acetyl tripeptide-30 citrulline to dilute the solution until the concentration of compound (II) is 150 μg / mL and the concentration of acetyl tripeptide-30 citrulline is 3 μg / mL.

[0216] Sample 7-5: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and acetyl tripeptide-30 citrulline at a concentration of 18 μg / mL. Specifically, the sample is obtained by mixing the basal medium solution with the stock solution containing compound (II) and acetyl tripeptide-30 citrulline to dilute the solution to a concentration of 150 μg / mL for compound (II) and 18 μg / mL for acetyl tripeptide-30 citrulline.

[0217] Sample 8-1: A DMEM culture medium solution containing compound (II) at a concentration of 150 μg / mL. Specifically, the sample is obtained by diluting the stock solution containing compound (II) with basal culture medium solution to a concentration of compound (II) of 150 μg / mL.

[0218] Sample 8-2: A DMEM medium solution containing palmitoyl pentapeptide-4 at a concentration of 0.3 μg / mL. Specifically, the sample is obtained by diluting the palmitoyl pentapeptide-4 stock solution with basal medium solution to a concentration of 0.3 μg / mL.

[0219] Sample 8-3: A DMEM medium solution containing palmitoyl pentapeptide-4 at a concentration of 3 μg / mL, 10% FBS and 1% penicillin / streptomycin. Specifically, the palmitoyl pentapeptide-4 stock solution was diluted with basal medium solution to a concentration of 3 μg / mL to obtain the sample.

[0220] Sample 8-4: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and palmitoyl pentapeptide-4 at a concentration of 0.3 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and the stock solution containing palmitoyl pentapeptide-4 to dilute the solution to a concentration of 150 μg / mL for compound (II) and a concentration of 0.3 μg / mL for palmitoyl pentapeptide-4.

[0221] Sample 8-5: A DMEM medium solution containing compound (II) at a concentration of 150 μg / mL and palmitoyl pentapeptide-4 at a concentration of 3 μg / mL. Specifically, the sample was obtained by mixing the basal medium solution with the stock solution containing compound (II) and the stock solution containing palmitoyl pentapeptide-4 to dilute the solution to a concentration of 150 μg / mL for compound (II) and a concentration of 3 μg / mL for palmitoyl pentapeptide-4.

[0222] <Experiment 1: Cytotoxicity Detection>

[0223] HaCaT cell viability was tested using the CCK8 (Cell Counting Kit) to detect the effect of the first to eighth compositions of the present disclosure on cells.

[0224] The test method includes the following steps S101 to S104:

[0225] Step S101: Cell seeding.

[0226] Specifically, immortalized keratinocytes (HaCaT) are taken and processed at a concentration of 1×10⁻⁶. 4 Inoculate the plates at a density of 100 μL / well into 96-well plates, add 100 μL of complete culture medium (complete culture medium is DMEM medium containing 10% FBS and 1% penicillin / streptomycin) to each well, and then incubate in an incubator (containing 5% CO2 at a temperature of 37°C) for 24 h.

[0227] Step S102, drug administration.

[0228] Specifically, when the cell seeding rate in the 96-well plate reaches 40%–50%, the cells are divided into a blank control group and at least one experimental group. 100 μL of the corresponding sample is added to each well of each group. After drug administration, the cells are placed in an incubator (37°C, 5% CO2) and cultured for 24 h.

[0229] Step S103, CCK8 detection.

[0230] After drug treatment, the cells were incubated for 24 hours, the supernatant was discarded, and 100 μL of CCK8 working solution was added (1 ml of CCK8 stock solution (Beyotime C0040 Cell Counting Kit-8) was added to 9 ml of DMEM to prepare 10 ml of CCK8 working solution). The cells were incubated at 37°C in the dark for 2 hours. After incubation, the OD value was read at 450 nm and the OD value was used as the relative viability of each group of cells.

[0231] Step S104: Calculate the cell viability of each experimental group.

[0232] The cell viability of the blank control group was set at 100% as a baseline to further determine the cell viability of each experimental group. The formula for calculating the cell viability of each experimental group is as follows:

[0233] Cell viability = [(OD experimental wells - OD zeroing wells) / (OD control wells - OD zeroing wells)] × 100%;

[0234] Among them, the OD experimental well is the absorbance value of the experimental group, the OD control well is the absorbance value of the blank control group, and the OD zeroing well is used to calculate the absorbance value of the control group.

[0235] The absorbance value of the control group can be determined as follows: Set up a cell-free well in a 96-well plate, add only CCK-8 working solution containing 1X, and read the OD value at 450 nm. This OD value will be used to calculate the absorbance value of the control group. Here, "X" refers to the concentration factor, and the same applies to any subsequent references to concentration.

[0236] <Experimental Example 1-1>

[0237] Experiment 1-1 was mainly used to verify the effect of the first composition on cell viability. The first composition included the compound shown in formula (I) and palmitoyl tripeptide-5. The mass ratio of the compound shown in formula (I) to palmitoyl tripeptide-5 was 12.5:(0.15-1.5), that is, 25:(0.3-3).

[0238] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells in the 96-well plate were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-1, experimental group 1-2, experimental group 1-3, experimental group 1-4 and experimental group 1-5. The samples added to the blank control group, experimental group 1-1, experimental group 1-2, experimental group 1-3, experimental group 1-4 and experimental group 1-5 were respectively: blank control group sample, sample 1-1, sample 1-2, sample 1-3, sample 1-4 and sample 1-5.

[0239] Experimental Results and Analysis

[0240] The experimental results are shown in Table 1-1.

[0241] Table 1-1

[0242] As shown in Table 1-1, the first composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0243] <Experimental Example 1-2>

[0244] Experimental Examples 1-2 were mainly used to verify the effect of the second composition on cell viability. The second composition included the compound shown in Formula (I) and acetyl dipeptide-1 cetyl ester. The mass ratio of the compound shown in Formula (I) to acetyl dipeptide-1 cetyl ester was 12.5:(0.25-2), that is, 25:(0.5-4).

[0245] The cell viability detection experiment was conducted according to the steps S101-104. In step S102, the cells in the 96-well plate were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-2-1, experimental group 1-2-2, experimental group 1-2-3, experimental group 1-2-4 and experimental group 1-2-5. The samples added to the blank control group, experimental group 1-2-1, experimental group 1-2-2, experimental group 1-2-3, experimental group 1-2-4 and experimental group 1-2-5 were blank control group sample, sample 2-1, sample 2-2, sample 2-3, sample 2-4 and sample 2-5, respectively.

[0246] Experimental Results and Analysis

[0247] The experimental results are shown in Table 1-2.

[0248] Table 1-2

[0249] As shown in Table 1-2, the second composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0250] <Experimental Examples 1-3>

[0251] Experiments 1-3 were mainly used to verify the effect of the third composition on cell viability. The third composition included the compound shown in formula (I) and acetyl tripeptide-30 citrulline. The mass ratio of the compound shown in formula (I) to acetyl tripeptide-30 citrulline was 12.5:(0.25-1.5), that is, 25:(0.5-3).

[0252] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells in the 96-well plate were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-3-1, experimental group 1-3-2, experimental group 1-3-3, experimental group 1-3-4 and experimental group 1-3-5. The samples added to the blank control group, experimental group 1-3-1, experimental group 1-3-2, experimental group 1-3-3, experimental group 1-3-4 and experimental group 1-3-5 were blank control group sample, sample 3-1, sample 3-2, sample 3-3, sample 3-4 and sample 3-5, respectively.

[0253] Experimental Results and Analysis

[0254] The experimental results are shown in Table 1-3.

[0255] Table 1-3

[0256] As shown in Table 1-3, the third composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0257] <Experimental Examples 1-4>

[0258] Experiments 1-4 were mainly used to verify the effect of the fourth composition on cell viability. The fourth composition included the compound shown in formula (I) and palmitoyl pentapeptide-4. The mass ratio of the compound shown in formula (I) to palmitoyl pentapeptide-4 was 12.5:(0.025-0.25), that is, 25:(0.05-0.5).

[0259] The cell viability detection experiment was conducted according to the steps S101-104. In step S102, the cells in the 96-well plate were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-4-1, experimental group 1-4-2, experimental group 1-4-3, experimental group 1-4-4 and experimental group 1-4-5. The samples added to the blank control group, experimental group 1-4-1, experimental group 1-4-2, experimental group 1-4-3, experimental group 1-4-4 and experimental group 1-4-5 were blank control group sample, sample 4-1, sample 4-2, sample 4-3, sample 4-4 and sample 4-5, respectively.

[0260] Experimental Results and Analysis

[0261] The experimental results are shown in Table 1-4.

[0262] Table 1-4

[0263] As shown in Table 1-4, the fourth composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0264] <Experimental Examples 1-5>

[0265] Examples 1-5 were mainly used to verify the effect of the fifth composition on cell viability. The fifth composition included the compound shown in formula (II) and palmitoyl tripeptide-5. The mass ratio of the compound shown in formula (II) to palmitoyl tripeptide-5 was 150:(1.8-18), that is, 25:(0.3-3).

[0266] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells in the 96-well plate were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-5-1, experimental group 1-5-2, experimental group 1-5-3, experimental group 1-5-4 and experimental group 1-5-5. The samples added to the blank control group, experimental group 1-5-1, experimental group 1-5-2, experimental group 1-5-3, experimental group 1-5-4 and experimental group 1-5-5 were respectively: blank control group sample, sample 5-1, sample 5-2, sample 5-3, sample 5-4 and sample 5-5.

[0267] Experimental Results and Analysis

[0268] The experimental results are shown in Table 1-5.

[0269] Table 1-5

[0270] As shown in Table 1-5, the fifth composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0271] <Experimental Examples 1-6>

[0272] Examples 1-6 were mainly used to verify the effect of the sixth composition on cell viability. The sixth composition included the compound shown in formula (II) and acetyl dipeptide-1 cetyl ester. The mass ratio of the compound shown in formula (II) to acetyl dipeptide-1 cetyl ester was 150:(3-24), that is, 25:(0.5-4).

[0273] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-6-1, experimental group 1-6-2, experimental group 1-6-3, experimental group 1-6-4 and experimental group 1-6-5. The samples added to the blank control group, experimental group 1-6-1, experimental group 1-6-2, experimental group 1-6-3, experimental group 1-6-4 and experimental group 1-6-5 were the blank control group sample, sample 6-1, sample 6-2, sample 6-3, sample 6-4 and sample 6-5, respectively.

[0274] Experimental Results and Analysis

[0275] The experimental results are shown in Table 1-6.

[0276] Table 1-6

[0277] As shown in Table 1-6, the first composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0278] <Experimental Examples 1-7>

[0279] Experiments 1-7 were mainly used to verify the effect of the seventh composition on cell viability. The seventh composition included the compound shown in formula (II) and acetyl tripeptide-30 citrulline. The mass ratio of the compound shown in formula (II) to acetyl tripeptide-30 citrulline was 150:(3-18), that is, 25:(0.5-3).

[0280] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-7-1, experimental group 1-7-2, experimental group 1-7-3, experimental group 1-7-4 and experimental group 1-7-5. The samples added to the blank control group, experimental group 1-7-1, experimental group 1-7-2, experimental group 1-7-3, experimental group 1-7-4 and experimental group 1-7-5 were the blank control group sample, sample 7-1, sample 7-2, sample 7-3, sample 7-4 and sample 7-5, respectively.

[0281] Experimental Results and Analysis

[0282] The experimental results are shown in Table 1-7.

[0283] Table 1-7

[0284] As shown in Table 1-7, the third composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0285] <Experimental Examples 1-8>

[0286] Experiments 1-8 were mainly used to verify the effect of the eighth composition on cell viability. The eighth composition included the compound shown in formula (II) and palmitoyl pentapeptide-4. The mass ratio of the compound shown in formula (II) to palmitoyl pentapeptide-4 was 150:(0.3-3), that is, 25:(0.05-0.5).

[0287] The experiment was conducted according to the cell viability detection method shown in steps S101-104. In step S102, the cells were divided into a blank control group and five experimental groups. The five experimental groups were experimental group 1-8-1, experimental group 1-8-2, experimental group 1-8-3, experimental group 1-8-4 and experimental group 1-8-5. The samples added to the blank control group, experimental group 1-8-1, experimental group 1-8-2, experimental group 1-8-3, experimental group 1-8-4 and experimental group 1-8-5 were the blank control group sample, sample 8-1, sample 8-2, sample 8-3, sample 8-4 and sample 8-5, respectively.

[0288] Experimental Results and Analysis

[0289] The experimental results are shown in Table 1-8.

[0290] Table 1-8

[0291] As shown in Tables 1-8, the eighth composition exhibits good cell survival rate and does not cause adverse effects on cells when applied to them.

[0292] <Experiment 2: mRNA Expression Detection>

[0293] Samples prepared according to the first to eighth compositions provided in the embodiments of this disclosure were used to treat HaCaT cells that had been treated with UVB irradiation. The mRNA expression level of the target gene (the target gene is the SLC7A11 gene or the HBGM1 gene) of the HaCaT cells was then detected to analyze the anti-UVB efficacy of the first to eighth compositions.

[0294] The experimental method includes the following steps S201 to S204.

[0295] S201, Cell Seeding:

[0296] Specifically, immortalized keratinocytes (HaCaT) were taken and processed at a concentration of 80 × 10⁻⁶. 4 Inoculate the plates at a density of 100 cells / well into 6-well plates, add 2000 μL of complete culture medium (complete culture medium is DMEM medium containing 10% FBS and 1% penicillin / streptomycin) to each well; and then incubate in an incubator (containing 5% CO2 at a temperature of 37°C) for 24 h.

[0297] S202, Drug administration:

[0298] When the cell seeding rate in the 6-well plate reaches 70%–80%, the cells are divided into a blank control group, a UVB control group, and at least one experimental group.

[0299] Except for the blank control group, the UVB control group and all experimental groups were treated with 50 mJ / cm². 2 Cells were irradiated with UVB dose; then the culture media of the blank control group, UVB control group and each experimental group were discarded, and the corresponding treatment was added to each group for drug administration. Each group was set with 5 replicates. After drug administration, the cells were placed in an incubator (37℃, 5% CO2) for 24h.

[0300] S203, RNA extraction:

[0301] After culturing for 24 hours, RNA was extracted from the cells in each group, specifically including the following steps S2031-S20310.

[0302] S2031. After culturing for 24 hours, pour out the culture medium and rinse once with PBS. Every 10cm... 2 Add 1 ml of TansZol Up to the growing cultured cells, place them horizontally for a moment to allow the lysis buffer to be evenly distributed on the cell surface and lyse the cells, then use a pipette to detach the cells. Transfer the cell lysis buffer to a centrifuge tube, add 0.2 ml of RNAExtractionAgent, and repeatedly pipette until there is no obvious precipitate in the lysis buffer. Vortex at room temperature for 5 minutes.

[0303] S2032. Centrifuge at 10,000g at 2℃~8℃ for 15 minutes. At this point, the sample separates into three layers: a colorless aqueous phase (upper layer), a middle layer, and a pink organic phase (lower layer); the RNA is in the aqueous phase, and the volume of the aqueous phase is approximately 50%~60% of the volume of the TransZol Up reagent used.

[0304] S2033. Transfer the colorless aqueous phase to a new centrifuge tube, add an equal volume of anhydrous ethanol, and gently invert to mix.

[0305] S2034. Add the obtained solution and precipitate together into a centrifuge column, centrifuge at 12,000g for 30 seconds at room temperature, and discard the eluent.

[0306] S2035, then add 500 μl of CB9 (Clean Buffer 9), centrifuge at 12,000 g for 30 seconds at room temperature, discard the eluent, and then repeat this step once.

[0307] S2036. Next, add 500 μl of WB9 (Wash Buffer 9), centrifuge at 12,000 g for 30 seconds at room temperature, discard the eluent, and repeat this step once.

[0308] S2037, centrifuge at 12,000g for 2 minutes at room temperature to completely remove residual ethanol.

[0309] S2038. Place the centrifuge column in an RNase-free tube, add 50-200 μl of RNase-free water to the center of the centrifuge column, and let it stand at room temperature for 1 minute.

[0310] S2039. Centrifuge at 12,000g for 1 minute at room temperature to elute RNA.

[0311] S20310. The concentration of RNA was determined using a micro spectrophotometer (Thermo Scientific NanoDrop), and the RNA samples with the measured concentrations were stored at -80℃.

[0312] S204. Perform qPCR on the RNA samples of each group with the measured concentration to determine the relative expression level of the target gene mRNA.

[0313] Step S204 specifically includes steps S2041 to S2043:

[0314] S2041. Reverse transcribe the RNA samples with measured concentrations in each group to obtain reverse transcribed samples.

[0315] Specifically, reverse transcription is performed using RT-PCR: the RNA sample with the measured concentration is used to calculate the corresponding RNA volume in 2 μg increments, and then the corresponding volume of RNase-free water (RNase-free H2O) and reverse transcriptase mix is ​​added. The total volume of the RT-PCR reaction system is 20 μL.

[0316] The specific system for the RT-PCR reaction can be found in Table 2-1, and the specific procedure for the RT-PCR reaction can be found in Table 2-2.

[0317] Table 2-1. RT-PCR reaction system

[0318] Table 2-2, Procedure for RT-PCR reaction

[0319] S2042. Then, the 20 μL reverse transcription sample was diluted to 400 μL to obtain a cDNA sample with a final concentration of 5 ng / μL.

[0320] S2043. Take cDNA samples and perform qPCR reaction to analyze the relative mRNA expression level of the corresponding test gene in each group.

[0321] Specifically, cDNA samples were used as cDNA templates for qPCR reactions. Three auxiliary wells were prepared for each gene in each cDNA sample for detection. After the samples were added, the qPCR program was run. After the qPCR reaction, the reaction data were processed, and the 2-ΔΔCt method was used to analyze the relative mRNA expression levels of the target genes in each group. The data between groups were analyzed using T-TEST. P < 0.05 indicated that the difference was statistically significant.

[0322] The volume of each well in the qPCR reaction system is 10 μL, as shown in Table 2-3.

[0323] The qPCR reaction procedure can be found in Table 2-4.

[0324] Table 2-3, qPCR reaction system

[0325] Table 2-4, qPCR reaction procedure

[0326] <Experimental Example 2-1>

[0327] Experimental Example 2-1 was mainly used to verify the anti-UVB damage effect of the first composition. The first composition includes the compound shown in Formula (I) and palmitoyl tripeptide-5. The mass ratio of the compound shown in Formula (I) to palmitoyl tripeptide-5 is 12.5:(0.15~1.5), that is, 25:(0.3~3).

[0328] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0329] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-1-1, experimental group 2-1-2, experimental group 2-1-3, experimental group 2-1-4, and experimental group 2-1-5. The samples added to the blank control group, UVB control group, experimental group 2-1-1, experimental group 2-1-2, experimental group 2-1-3, experimental group 2-1-4, and experimental group 2-1-5 are respectively: blank control group sample, UVB control group sample, sample 1-1, sample 1-2, sample 1-3, sample 1-4, and sample 1-5.

[0330] In addition, the target gene for each group in the experiment was the HBGM1 gene.

[0331] Experimental results and analysis:

[0332] After obtaining the relative expression level (i.e., relative expression amount) of HBGM1 in each group, the expression inhibition rate (%) of HBGM1 in each experimental group relative to the UVB control group was calculated according to Equation (a).

[0333] Equation (a) is:

[0334] The inhibition rate of HBGM1 expression (%) = (relative expression level of HBGM1 in the experimental group - relative expression level of HBGM1 in the UVB control group) / relative expression level of HBGM1 in the UVB control group.

[0335] When calculating according to equation (a), the relative expression level of HBGM1 is taken as the average value and substituted into the calculation.

[0336] The experimental results are shown in Table 2-5.

[0337] Table 2-5

[0338] From the above results, we can conclude that:

[0339] Compared to the UVB control group, when compound (I) at a concentration of 12.5 μg / mL was used alone in experimental group 2-1-1, the expression of HBGM1 was inhibited by approximately 16.51%.

[0340] Compared to the UVB control group, when palmitoyl tripeptide-5 was used alone in experimental groups 2-1-2 and 2-1-3 at concentrations of 0.15 μg / mL and 1.5 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 3.21% and 8.21%, respectively.

[0341] According to the comparison results of experimental groups 2-1-4 and 2-1-5 with the UVB control group, when compound of formula (I) at 12.5 μg / mL was combined with palmitoyl tripeptide-5 at concentrations of 0.15 μg / mL and 1.5 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 48% and 32%, respectively.

[0342] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the first composition containing the compound shown in formula (I) and palmitoyl tripeptide-5 can significantly inhibit the expression of HBGM1 and reduce the damage of UVB irradiation to the skin.

[0343] <Experimental Example 2-2>

[0344] Experimental Example 2-2 was mainly used to verify the UVB damage resistance effect of the second composition. The second composition included the compound shown in Formula (I) and acetyl dipeptide-1 cetyl ester. The mass ratio of the compound shown in Formula (I) to acetyl dipeptide-1 cetyl ester was 12.5:(0.25-2), or 25:(0.5-4).

[0345] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0346] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-2-1, experimental group 2-2-2, experimental group 2-2-3, experimental group 2-2-4, and experimental group 2-2-5. The samples added to the blank control group, UVB control group, experimental group 2-1, experimental group 2-2-2, experimental group 2-2-3, experimental group 2-2-4, and experimental group 2-2-5 are respectively: blank control group sample, UVB control group sample, sample 2-1, sample 2-2, sample 2-3, sample 2-4, and sample 2-5.

[0347] In addition, the target gene for each group in the experiment was the HBGM1 gene.

[0348] Experimental results and analysis:

[0349] After obtaining the relative expression level (i.e., relative expression amount) of HBGM1 in each group, the expression inhibition rate (%) of HBGM1 in each experimental group relative to the UVB control group was calculated according to Equation (a).

[0350] Equation (a) is:

[0351] The inhibition rate of HBGM1 expression (%) = (relative expression level of HBGM1 in the experimental group - relative expression level of HBGM1 in the UVB control group) / relative expression level of HBGM1 in the UVB control group.

[0352] When calculating according to equation (a), the relative expression level of HBGM1 is taken as the average value and substituted into the calculation.

[0353] The experimental results are shown in Table 2-6.

[0354] Table 2-6

[0355] From the above results, we can conclude that:

[0356] Compared to the UVB control group, when compound (I) of formula was used alone at a concentration of 12.5 μg / mL in experimental group 2-2-1, the expression of HMGB1 was inhibited by approximately 14.69%.

[0357] Compared with the UVB control group, when acetyl dipeptide-1 cetyl ester at concentrations of 0.25 μg / mL and 2.0 μg / mL were used alone in experimental groups 2-2-2 and 2-2-3, respectively, the expression of HMGB1 was inhibited by approximately 13.74% and 12.8%, respectively.

[0358] According to the comparison results of experimental groups 2-2-4 and 2-2-5 with the UVB control group, when compound of formula (I) at a concentration of 12.5 μg / mL was combined with acetyl dipeptide-1 cetyl ester at concentrations of 0.25 μg / mL and 2.0 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 48% and 61%.

[0359] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the second composition containing the compound shown in formula (I) and acetyl dipeptide-1 cetyl ester can significantly inhibit the expression of HBGM1 and reduce the damage of UVB irradiation to the skin.

[0360] <Experimental Example 2-3>

[0361] Experimental Examples 2-3 were mainly used to verify the anti-UVB damage effect of the third composition. The third composition included the compound shown in Formula (I) and acetyl tripeptide-30 citrulline. The mass ratio of the compound shown in Formula (I) to acetyl tripeptide-30 citrulline was 12.5:(0.25-1.5), or 25:(0.5-3).

[0362] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0363] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-3-1, experimental group 2-3-2, experimental group 2-3-3, experimental group 2-3-4, and experimental group 2-3-5. The samples added to the blank control group, UVB control group, experimental group 2-3-1, experimental group 2-3-2, experimental group 2-3-3, experimental group 2-3-4, and experimental group 2-3-5 are respectively: blank control group sample, UVB control group sample, sample 3-1, sample 3-2, sample 3-3, sample 3-4, and sample 3-5.

[0364] In addition, the target gene for each group in the experiment was the HBGM1 gene.

[0365] Experimental results and analysis:

[0366] After obtaining the relative expression level (i.e., relative expression amount) of HBGM1 in each group, the expression inhibition rate (%) of HBGM1 in each experimental group relative to the UVB control group was calculated according to Equation (a).

[0367] Equation (a) is:

[0368] The inhibition rate of HBGM1 expression (%) = (relative expression level of HBGM1 in the experimental group - relative expression level of HBGM1 in the UVB control group) / relative expression level of HBGM1 in the UVB control group.

[0369] When calculating according to equation (a), the relative expression level of HBGM1 is taken as the average value and substituted into the calculation.

[0370] The experimental results are shown in Table 2-7.

[0371] Table 2-7

[0372] From the above, we can see that:

[0373] Compared to the UVB control group, when compound (I) at a concentration of 12.5 μg / mL was used alone in experimental group 2-3-1, the expression of HBGM1 was inhibited by approximately 13.02%.

[0374] Compared to the UVB control group, when HBGM1 expression was inhibited by approximately 5.42% and 8.02% in experimental groups 2-3-2 and 2-3-3 alone, with concentrations of 0.25 μg / mL and 1.5 μg / mL, respectively.

[0375] According to the comparison results of experimental groups 2-3-4 and 2-3-5 with the UVB control group, when compound of formula (I) at 12.5 μg / mL was combined with acetyl tripeptide-30 citrulline at concentrations of 0.25 μg / mL and 1.5 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 40% and 35%.

[0376] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the first composition containing the compound shown in formula (I) and acetyl tripeptide-30 citrulline can significantly inhibit the expression of HBGM1 and reduce the damage of UVB irradiation to the skin.

[0377] <Experimental Example 2-4>

[0378] Experimental Examples 2-4 were mainly used to verify the anti-UVB damage effect of the fourth composition. The fourth composition included the compound shown in Formula (I) and palmitoyl pentapeptide-4. The mass ratio of the compound shown in Formula (I) to palmitoyl pentapeptide-4 was 12.5:(0.025-0.25), that is, 25:(0.05-0.5).

[0379] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0380] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-4-1, experimental group 2-4-2, experimental group 2-4-3, experimental group 2-4-4, and experimental group 2-4-5. The samples added to the blank control group, UVB control group, experimental group 2-4-1, experimental group 2-4-2, experimental group 2-4-3, experimental group 2-4-4, and experimental group 2-4-5 are respectively: blank control group sample, UVB control group sample, sample 4-1, sample 4-2, sample 4-3, sample 4-4, and sample 4-5.

[0381] In addition, the target gene for each group in the experiment was the HBGM1 gene.

[0382] Experimental results and analysis:

[0383] After obtaining the relative expression level (i.e., relative expression amount) of HBGM1 in each group, the expression inhibition rate (%) of HBGM1 in each experimental group relative to the UVB control group was calculated according to Equation (a).

[0384] Equation (a) is:

[0385] The inhibition rate of HBGM1 expression (%) = (relative expression level of HBGM1 in the experimental group - relative expression level of HBGM1 in the UVB control group) / relative expression level of HBGM1 in the UVB control group.

[0386] When calculating according to equation (a), the relative expression level of HBGM1 is taken as the average value and substituted into the calculation.

[0387] The experimental results are shown in Table 2-8.

[0388] Table 2-8

[0389] From the above results, we can conclude that:

[0390] Compared to the UVB control group, when compound (I) at a concentration of 12.5 μg / mL was used alone in experimental group 2-4-1, the expression of HBGM1 was inhibited by approximately 17.57%.

[0391] Compared with the UVB control group, when palmitoyl pentapeptide-4 was used alone in experimental groups 2-4-2 and 2-4-3 at concentrations of 0.025 μg / mL and 0.25 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 19.22% and 5.32%, respectively.

[0392] According to the comparison results of experimental groups 2-4-4 and 2-4-5 with the UVB control group, when compound of formula (I) at 12.5 μg / mL was combined with palmitoyl pentapeptide-4 at concentrations of 0.025 μg / mL and 0.25 μg / mL, respectively, the expression of HBGM1 was inhibited by approximately 56% and 45%.

[0393] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the first composition containing the compound shown in formula (I) and palmitoyl pentapeptide-4 can significantly inhibit the expression of HBGM1 and reduce the damage of UVB irradiation to the skin.

[0394] In summary, UVB irradiation significantly increased the expression level of HBGM1. However, within specific ratios, combining compound (I) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 significantly reduced HBGM1 expression levels. Furthermore, the combination of compound (I) and palmitoyl tripeptide-5 exhibited additional synergistic effects compared to using compound (I) or palmitoyl tripeptide-5 alone.

[0395] Therefore, the combination of compound (I) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 can significantly reduce the expression level of HBGM1, indicating that the combination of compound (I) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 can be particularly effective in resisting DNA damage caused by UVB.

[0396] <Experimental Example 2-5>

[0397] Experimental Examples 2-5 were mainly used to verify the anti-UVB damage effect of the fifth composition. The fifth composition included the compound shown in Formula (II) and palmitoyl tripeptide-5. The mass ratio of the compound shown in Formula (II) to palmitoyl tripeptide-5 was 150:(1.8-18), that is, 25:(0.3-3).

[0398] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0399] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-5-1, experimental group 2-5-2, experimental group 2-5-3, experimental group 2-5-4, and experimental group 2-5-5. The samples added to the blank control group, UVB control group, experimental group 2-5-1, experimental group 2-5-2, experimental group 2-5-3, experimental group 2-5-4, and experimental group 2-5-5 are respectively: blank control group sample, UVB control group sample, sample 5-1, sample 5-2, sample 5-3, sample 5-4, and sample 5-5.

[0400] In addition, the target gene for each group in the experiment was the SLC7A11 gene.

[0401] Experimental results and analysis:

[0402] After obtaining the relative expression level (i.e., relative expression amount) of SLC7A11 in each group, the expression enhancement rate (%) of SLC7A11 in each experimental group relative to the UVB control group was calculated according to Equation (b).

[0403] Equation (b) is:

[0404] The expression enhancement rate (%) of SLC7A11 = (relative expression level of SLC7A11 in the experimental group - relative expression level of SLC7A11 in the UVB control group) / relative expression level of SLC7A11 in the UVB control group.

[0405] When calculating according to equation (b), the relative expression level of SLC7A11 is taken as the average value and substituted into the calculation.

[0406] The experimental results are shown in Table 2-9.

[0407] Table 2-9

[0408] From the above results, we can conclude that:

[0409] Compared to the UVB treatment group, SLC7A11 expression was increased by approximately 3% when compound (II) at a concentration of 150 μg / mL was used alone.

[0410] Compared to the UVB treatment group, the expression of SLC7A11 was increased by approximately 34% and decreased by approximately 6% when palmitoyl tripeptide-5 was used alone at concentrations of 1.8 μg / mL and 18 μg / mL, respectively.

[0411] When compound (II) at a concentration of 150 μg / mL was combined with palmitoyl tripeptide-5 at concentrations of 1.8 μg / mL and 18 μg / mL, SLC7A11 expression was significantly increased to approximately 88.57% and 85.71%, respectively.

[0412] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the fifth composition containing the compound shown in formula (II) and palmitoyl tripeptide-5 can significantly increase the expression rate of HBGM1, promote the expression of HBGM1, and reduce the damage of UVB irradiation to the skin.

[0413] <Experimental Example 2-6>

[0414] Experimental Examples 2-6 were mainly used to verify the UVB damage resistance effect of the sixth composition. The sixth composition included the compound shown in Formula (II) and acetyl dipeptide-1 cetyl ester. The mass ratio of the compound shown in Formula (II) to acetyl dipeptide-1 cetyl ester was 150:(3-24), that is, 25:(0.5-4).

[0415] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0416] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-6-1, experimental group 2-6-2, experimental group 2-6-3, experimental group 2-6-4, and experimental group 2-6-5. The samples added to the blank control group, UVB control group, experimental group 2-6-1, experimental group 2-6-2, experimental group 2-6-3, experimental group 2-6-4, and experimental group 2-6-5 are respectively: blank control group sample, UVB control group sample, sample 6-1, sample 6-2, sample 6-3, sample 6-4, and sample 6-5.

[0417] In addition, the target gene for each group in the experiment was the SLC7A11 gene.

[0418] Experimental results and analysis:

[0419] After obtaining the relative expression level (i.e., relative expression amount) of SLC7A11 in each group, the expression enhancement rate (%) of SLC7A11 in each experimental group relative to the UVB control group was calculated according to Equation (b).

[0420] Equation (b) is:

[0421] The expression enhancement rate (%) of SLC7A11 = (relative expression level of SLC7A11 in the experimental group - relative expression level of SLC7A11 in the UVB control group) / relative expression level of SLC7A11 in the UVB control group.

[0422] When calculating according to equation (b), the relative expression level of SLC7A11 is taken as the average value and substituted into the calculation.

[0423] The experimental results are shown in Table 2-10.

[0424] Table 2-10

[0425] The results above show that, compared to the UVB treatment group, the expression of SLC7A11 decreased by 3% when compound (II) at a concentration of 150 μg / mL was used alone.

[0426] Compared to the UVB treatment group, SLC7A11 expression was reduced when acetyl dipeptide-1 cetyl ester was used alone at concentrations of 3 μg / mL and 24 μg / mL.

[0427] When compound of formula (II) at a concentration of 150 μg / mL was used in combination with acetyl dipeptide-1 cetyl ester at concentrations of 3 μg / mL and 24 μg / mL, the expression of SLC7A11 was significantly increased to approximately 26.3% and 39.5%, respectively.

[0428] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the sixth composition containing the compound shown in formula (II) and acetyl dipeptide-1 cetyl ester can significantly increase the expression rate of HBGM1, promote the expression of HBGM1, and reduce the damage of UVB irradiation to the skin.

[0429] <Experimental Example 2-7>

[0430] Experimental Examples 2-7 were mainly used to verify the anti-UVB damage effect of the seventh composition. The seventh composition includes the compound shown in Formula (II) and acetyl tripeptide-30 citrulline. The mass ratio of the compound shown in Formula (II) to acetyl tripeptide-30 citrulline is 150:(3-18), that is, 25:(0.5-3).

[0431] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0432] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-7-1, experimental group 2-7-2, experimental group 2-7-3, experimental group 2-7-4, and experimental group 2-7-5. The samples added to the blank control group, UVB control group, experimental group 2-7-1, experimental group 2-7-2, experimental group 2-7-3, experimental group 2-7-4, and experimental group 2-7-5 are respectively: blank control group sample, UVB control group sample, sample 7-1, sample 7-2, sample 7-3, sample 7-4, and sample 7-5.

[0433] In addition, the target gene for each group in the experiment was the SLC7A11 gene.

[0434] Experimental results and analysis:

[0435] After obtaining the relative expression level (i.e., relative expression amount) of SLC7A11 in each group, the expression enhancement rate (%) of SLC7A11 in each experimental group relative to the UVB control group was calculated according to Equation (b).

[0436] Equation (b) is:

[0437] The expression enhancement rate (%) of SLC7A11 = (relative expression level of SLC7A11 in the experimental group - relative expression level of SLC7A11 in the UVB control group) / relative expression level of SLC7A11 in the UVB control group.

[0438] When calculating according to equation (b), the relative expression level of SLC7A11 is taken as the average value and substituted into the calculation.

[0439] The experimental results are shown in Table 2-11.

[0440] Table 2-11

[0441] Compared to the UVB treatment group, SLC7A11 expression was increased by 6% when compound (II) at a concentration of 150 μg / mL was used alone.

[0442] Compared to the UVB treatment group, the expression of SLC7A11 was increased by 10% and 23% when acetyl tripeptide-30 citrulline was used alone at concentrations of 3 μg / mL and 18 μg / mL, respectively.

[0443] When compound of formula (I) at a concentration of 150 μg / mL was combined with acetyl tripeptide-30 citrulline at concentrations of 3 μg / mL and 18 μg / mL, the expression of SLC7A11 was significantly increased to approximately 65% ​​and 52%, respectively.

[0444] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the seventh composition containing the compound shown in formula (II) and acetyl tripeptide-30 citrulline can significantly increase the expression rate of HBGM1, promote the expression of HBGM1, and reduce the damage of UVB irradiation to the skin.

[0445] <Experimental Example 2-8>

[0446] Experimental Examples 2-8 were mainly used to verify the anti-UVB damage effect of the eighth composition. The eighth composition included the compound shown in Formula (II) and palmitoyl pentapeptide-4. The mass ratio of the compound shown in Formula (II) to palmitoyl pentapeptide-4 was 150:(0.3-3), that is, 25:(0.05-0.5).

[0447] The experiment was conducted according to the experimental methods shown in steps S201 to S204 above; wherein...

[0448] In step S202, the cells are divided into a blank control group, a UVB control group, and five experimental groups. The five experimental groups are experimental group 2-8-1, experimental group 2-8-2, experimental group 2-8-3, experimental group 2-8-4, and experimental group 2-8-5. The samples added to the blank control group, UVB control group, experimental group 2-8-1, experimental group 2-8-2, experimental group 2-8-3, experimental group 2-8-4, and experimental group 2-8-5 are respectively: blank control group sample, UVB control group sample, sample 8-1, sample 8-2, sample 8-3, sample 8-4, and sample 8-5.

[0449] In addition, the target gene for each group in the experiment was the SLC7A11 gene.

[0450] Experimental results and analysis:

[0451] After obtaining the relative expression level (i.e., relative expression amount) of SLC7A11 in each group, the expression enhancement rate (%) of SLC7A11 in each experimental group relative to the UVB control group was calculated according to Equation (b).

[0452] Equation (b) is:

[0453] The expression enhancement rate (%) of SLC7A11 = (relative expression level of SLC7A11 in the experimental group - relative expression level of SLC7A11 in the UVB control group) / relative expression level of SLC7A11 in the UVB control group.

[0454] When calculating according to equation (b), the relative expression level of SLC7A11 is taken as the average value and substituted into the calculation.

[0455] The experimental results are shown in Table 2-12.

[0456] Table 2-12

[0457] From the above results, we can conclude that:

[0458] Compared to the UVB treatment group, SLC7A11 expression was increased by 5% when compound (II) at a concentration of 150 μg / mL was used alone.

[0459] Compared with the UVB treatment group, the expression of SLC7A11 was increased by 13% and 8% when palmitoyl pentapeptide-4 was used alone at concentrations of 0.3 μg / mL and 3 μg / mL, respectively.

[0460] When compound of formula (II) at a concentration of 150 μg / mL was combined with palmitoyl pentapeptide-4 at concentrations of 0.3 μg / mL and 3 μg / mL, the expression of SLC7A11 was significantly increased to approximately 74% and 87%, respectively.

[0461] As can be seen from the above, for skin cells (HaCaT cells) exposed to UVB, the seventh composition containing the compound shown in formula (II) and acetyl tripeptide-30 citrulline can significantly increase the expression rate of HBGM1, promote the expression of HBGM1, and reduce the damage of UVB irradiation to the skin.

[0462] In summary, UVB irradiation significantly reduced the expression level of SLC7A11 in skin cells (HaCaT cells). However, the combined use of compound (II) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 within specific ratios significantly increased the expression level of SLC7A11. Moreover, the combination of compound (II) and palmitoyl tripeptide-5 exhibited additional synergistic effects compared to the use of compound (II) or palmitoyl tripeptide-5 alone.

[0463] Therefore, the combination of compound (II) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 can significantly improve the expression level of SLC7A11, indicating that the combination of compound (II) with palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4 can be particularly effective in resisting UVB-induced oxidative stress.

[0464] <Application Example>

[0465] The compositions provided in this disclosure can be used to prepare skin care products in the form of emulsions.

[0466] In an application example, this disclosure provides an emulsion that can be prepared according to the components and their contents in the emulsion formulations shown in Tables 3-1 to 3-8, using the following emulsion preparation method.

[0467] Emulsion preparation method:

[0468] Phase A was heated to 85°C and swollen uniformly, while phase B was heated to 85°C and dissolved uniformly.

[0469] After adding the uniformly swollen phase A to the uniformly dissolved phase B and homogenizing for 2-3 minutes, the first mixture is obtained.

[0470] Add C phase homogenization to the first mixture for 1-2 minutes to obtain the second mixture;

[0471] The second mixture is stirred and cooled to below 40°C. Then, phase D and the dissolved phase E are added and stirred evenly. The emulsion is obtained after discharge.

[0472] Table 3-1, Emulsion Formulation 1

[0473] Table 3-2, Emulsion Formulation 2

[0474] Table 3-3, Emulsion Formulation 3

[0475] Table 3-4, Emulsion Formulation 4

[0476] Table 3-5, Emulsion Formulation 5

[0477] Table 3-6, Emulsion Formulation 6

[0478] Table 3-7, Emulsion Formulation 7

[0479] Table 3-8, Emulsion Formulation 8

[0480] The emulsions prepared above all contain the first compound and the second compound, and therefore have the effects and uses of the composition described above.

[0481] The above detailed embodiments provide a comprehensive description of this disclosure, but they do not constitute a limitation thereof. The scope of protection of this disclosure is not limited to the above embodiments; any equivalent modifications or variations made by those skilled in the art based on the content disclosed herein should be included within the scope of protection set forth in the claims. Industrial applicability

[0482] The composition disclosed herein has anti-UVB damage function and can be used to solve the problem of anti-UVB damage. For example, it can reduce the expression level of HMGB1 in keratinocytes after UVB irradiation and increase the expression level of SLC7A11 in keratinocytes after UVB irradiation, thereby achieving anti-inflammatory effects and playing a role in resisting UVB damage.

Claims

1. A composition having anti-UVB damage function, characterized in that, include: The first compound is selected from the compounds represented by formula (I) or formula (II); Equation (I): Equation (II): and The second compound includes any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

2. The composition according to claim 1, characterized in that, The second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

3. The composition according to claim 1 or 2, characterized in that, The first compound is the compound shown in formula (I), and the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (I) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or The first compound is the compound shown in formula (I), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (I) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or The first compound is the compound shown in formula (I), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (I) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or The first compound is the compound shown in formula (I), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (I) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.

5.

4. The composition according to claim 1 or 2, characterized in that, The first compound is the compound represented by formula (II); the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (II) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or The first compound is the compound shown in formula (II), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (II) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or The first compound is the compound shown in formula (II), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (II) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or The first compound is the compound shown in formula (II), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (II) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.

5.

5. The composition according to any one of claims 1 to 4, characterized in that, It also includes solvents.

6. A skincare product, characterized in that, include: The first compound is selected from the compounds represented by formula (I) or formula (II); Equation (I): Equation (II): and The second compound includes any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

7. The skincare product according to claim 6, characterized in that, The second compound is selected from any one of palmitoyl tripeptide-5, acetyl dipeptide-1 cetyl ester, acetyl tripeptide-30 citrulline, and palmitoyl pentapeptide-4.

8. The skincare product according to claim 6 or 7, characterized in that, The first compound is the compound shown in formula (I), and the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (I) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or The first compound is the compound shown in formula (I), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (I) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or The first compound is the compound shown in formula (I), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (I) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or The first compound is the compound shown in formula (I), and the second compound is palmitoyl pentapeptide-4, with a mass ratio of the compound of formula (I) to palmitoyl pentapeptide-4 of 25:0.05 to 25:0.

5.

9. The skincare product according to claim 6 or 7, characterized in that, The first compound is the compound represented by formula (II); the second compound is palmitoyl tripeptide-5, wherein the mass ratio of the compound of formula (II) to palmitoyl tripeptide-5 is 25:0.3 to 25:3; or The first compound is the compound shown in formula (II), and the second compound is acetyl dipeptide-1 cetyl ester, wherein the mass ratio of the compound of formula (II) to acetyl dipeptide-1 cetyl ester is 25:0.5 to 25:4; or The first compound is the compound shown in formula (II), and the second compound is acetyl tripeptide-30-citrulline, wherein the mass ratio of the compound of formula (II) to acetyl tripeptide-30-citrulline is 25:0.5 to 25:3; or The first compound is the compound shown in formula (II), and the second compound is palmitoyl pentapeptide-4, with the mass ratio of the compound of formula (II) to palmitoyl pentapeptide-4 being 25:0.05 to 25:0.

5.

10. Use of the composition according to any one of claims 1 to 5 in the preparation of an anti-UVB damage formulation.

11. Use of the composition according to any one of claims 1 to 5 in the preparation of DNA damage inhibitors.

12. Use of the composition according to any one of claims 1 to 3 in the preparation of an HMGB1 expression inhibitor.

13. Use of the composition according to claim 1, 2 or 4 in the preparation of an SLC7A11 expression promoter.

14. Use of the composition according to any one of claims 1 to 5 in the preparation of skin care products.

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