Composition for improving skin renewal cycle containing compound k

Abstract

The present disclosure relates to a composition for improving skin renewal cycle containing Compound K. Specifically, the composition for improving skin renewal cycle according to the present disclosure is capable of continuously self-replicating keratinocytes by increasing the expression of p63 and KLF4, which are markers related to keratinization function and dryness in the epidermal layer, and is capable of continuously forming keratin by promoting cell division, thereby being capable of effectively repairing the skin renewal cycle that is lengthened due to the inhibition of epidermal cell proliferation.

Description

Technical Field

[0001] This disclosure relates to a composition containing compound K for improving the skin renewal cycle. Cross-reference to related applications

[0002] This application claims priority to Korean Patent Application No. 10-2024-0045898, filed on April 4, 2024, the entire contents of which are incorporated herein by reference. Background Technology

[0003] As skin tissue ages, inflammatory responses increase, and external stimuli such as UVB, dust, and blue light (high-energy visible light) are known to induce skin aging. These external stimuli are thought to further accelerate responses that arise from natural aging.

[0004] The epidermis maintains a skin turnover cycle through continuous keratinization and shedding. When this cycle becomes shorter or longer, normal epidermal functions, including the skin's defense against stimuli, are compromised. The skin turnover cycle involves the proliferation and differentiation of keratinocytes in the basal layer, which rise to the stratum corneum to form new keratinocytes and shed the existing ones, repeating this process. Keratinocyte proliferation is a crucial factor regulating the skin turnover cycle. When keratinocytes age due to inflammation or external stimuli, their self-replicating ability decreases, and their proliferative capacity declines, leading to an inability to form new keratinocytes. This results in a thinner epidermis and ultimately a longer skin turnover cycle.

[0005] Therefore, in order to improve the skin renewal cycle, it is necessary to improve the proliferation capacity of keratinocytes, thereby enhancing the ability to generate keratin.

[0006] [Existing Technical Documents]

[0007] [Patent Documents]

[0008] (Patent Document 1) Korean Patent Publication No. 10-2014-0003198 Summary of the Invention

[0009] Technical issues

[0010] This disclosure aims to provide a composition that, by increasing the expression of p63 and KLF4, which are markers of keratinization function and dryness in the epidermis, enables keratinocytes to continuously self-replicate and continuously form keratin by promoting cell division, thereby effectively repairing the prolonged skin renewal cycle caused by the inhibition of epidermal cell proliferation.

[0011] Technical solution

[0012] To achieve the aforementioned objective, one embodiment of the present invention provides a composition containing compound K for improving the skin renewal cycle.

[0013] Invention Effects

[0014] According to the composition disclosed herein for improving the skin renewal cycle, by increasing the expression of p63 and KLF4, which are markers related to keratinization function and dryness in the epidermis, keratinocytes can continuously self-replicate and continuously form keratin by promoting cell division, thereby effectively repairing the skin renewal cycle that has been prolonged due to the inhibition of epidermal cell proliferation. Attached Figure Description

[0015] Figure 1 The results of skin cell toxicity experiments for compound K are shown.

[0016] Figure 2a and Figure 2b The results show the changes in p63 and KLF4 expression in an environment of accelerated skin aging caused by UVB treatment.

[0017] Figure 3a and Figure 3b The results show the changes in the expression of p63 and KLF4 in an environment where skin aging is accelerated by particulate matter (PM2.5) treatment.

[0018] Figure 4a and Figure 4b The results show the changes in the expression of p63 and KLF4 under conditions of accelerated skin aging caused by blue light (HEV) treatment.

[0019] Figures 5a to 5c Results confirming the efficacy of compound K in artificial skin that exhibits accelerated skin aging caused by UVB treatment. Detailed Implementation

[0020] The present invention will now be described in detail.

[0021] In one aspect, the present invention may relate to a composition containing compound K for improving the skin renewal cycle.

[0022] In one aspect, the present invention may relate to a method for improving the skin renewal cycle, the method comprising the step of applying or administering an effective amount of compound K to a subject in need.

[0023] In one aspect, the present invention may relate to the use of compound K for preparing compositions for improving the skin renewal cycle.

[0024] In one aspect, the present invention may relate to a compound K used for improving the skin renewal cycle.

[0025] In one aspect, the present invention may relate to the non-therapeutic use of compound K for improving the skin renewal cycle.

[0026] The "skin turnover cycle," the cell cycle occurring in the epidermis, the outermost layer of the skin, refers to the process by which keratinocytes proliferate and differentiate in the basal layer, the deepest layer of the epidermis, rise to the stratum corneum to form new stratum corneum and accumulate, and then the existing stratum corneum is shed, continuing until shedding. Epidermal turnover is affected by the rate of new epidermal cell formation and the rate of keratinocyte shedding, both of which are known to decrease with age. When the epidermal turnover cycle becomes prolonged due to insufficient new cell formation or inadequate keratinocyte shedding, the skin barrier function, a representative function of the epidermis, will not function properly. Therefore, to ensure normal epidermal function, it is necessary to maintain the skin turnover cycle, and to improve the skin turnover cycle, it is important to normalize the rate of new epidermal cell formation.

[0027] In one embodiment, the compound K may be represented by the following chemical formula 1.

[0028]

Chemical Formula 1

[0029]

[0030] In one embodiment, the compound K may contain an amount of 0.0002 to 0.04% by weight relative to the total weight of the composition. Specifically, the compound K may contain an amount of 0.0002% or more by weight, 0.0003% or more by weight, 0.0004% or more by weight, 0.0005% or more by weight, 0.0006% or more by weight, 0.0007% or more by weight, 0.0008% or more by weight, 0.0009% or more by weight, 0.001% or more by weight, 0.002% or more by weight, 0.003% or more by weight, 0.004% or more by weight, 0.005% or more by weight, 0.006% or more by weight, 0.007% or more by weight, 0.008% or more by weight, 0.009% or more by weight, 0.01% or more by weight, or 0.02% or more by weight relative to the total weight of the composition. The compound K may be present in amounts of less than 0.04 wt%, less than 0.03 wt%, less than 0.02 wt%, less than 0.01 wt%, less than 0.009 wt%, less than 0.008 wt%, less than 0.007 wt%, less than 0.006 wt%, less than 0.005 wt%, less than 0.004 wt%, less than 0.003 wt%, less than 0.002 wt%, less than 0.001 wt%, less than 0.0009 wt%, less than 0.0008 wt%, less than 0.0007 wt%, less than 0.0006 wt%, less than 0.0005 wt%, less than 0.0004 wt%, or less than 0.0003 wt%, relative to the total weight of the composition.

[0031] In one embodiment, compound K can increase the expression of p63.

[0032] In one embodiment, the compound K can increase the expression of KLF4.

[0033] p63, a marker regulating keratinocyte division and differentiation, is reduced when its levels are low, inhibiting keratinocyte division and thus hindering keratin formation. KLF4, a marker associated with dryness, is reduced when its levels are low, indicating decreased cell dryness. When both p63 and KLF4 are reduced in skin keratinocytes, it indicates a loss of proliferative function in the epidermis. Therefore, regulating the expression of p63 and KLF4 is crucial for regulating the skin renewal cycle in the epidermis.

[0034] In one embodiment, compound K can increase the expression of one or more of p63 and KLF4 in keratinocytes of the epidermis.

[0035] In one embodiment, the compound K can improve the skin renewal cycle in the epidermis by increasing the expression of more than one of p63 and KLF4.

[0036] In one embodiment, the compound K can restore the elongated skin renewal cycle in the epidermis by increasing the expression of one or more of p63 and KLF4.

[0037] In one embodiment, the daily dosage of compound K may be from 0.5 mg / kg (body weight) to 10 mg / kg (body weight). Specifically, the daily dosage, topical application, or intake of compound K can be 0.5 mg / kg (body weight) or more, 1 mg / kg (body weight) or more, 1.5 mg / kg (body weight) or more, 2 mg / kg (body weight) or more, 2.5 mg / kg (body weight) or more, 3 mg / kg (body weight) or more, 3.5 mg / kg (body weight) or more, 4 mg / kg (body weight) or more, 4.5 mg / kg (body weight) or more, 5 mg / kg (body weight) or more, 5.5 mg / kg (body weight) or more, 6 mg / kg (body weight) or more, 6.5 mg / kg (body weight) or more, 7 mg / kg (body weight) or more, 7.5 mg / kg (body weight) or more, 8 mg / kg (body weight) or more, 8.5 mg / kg (body weight) or more, 9 mg / kg (body weight) or more, or 9.5 mg / kg (body weight) or more. Alternatively, the daily dosage of compound K can be less than 10 mg / kg (body weight), less than 9.5 mg / kg (body weight), or less than 9 mg / kg (body weight). mg / kg (body weight) or less, 8.5 mg / kg (body weight) or less, 8 mg / kg (body weight) or less, 7.5 mg / kg (body weight) or less, 7 mg / kg (body weight) or less, 6.5 mg / kg (body weight) or less, 6 mg / kg (body weight) or less, 5.5 mg / kg (body weight) or less, 5 mg / kg (body weight) or less, 4.5 mg / kg (body weight) or less, 4 mg / kg (body weight) or less, 3.5 mg / kg (body weight) or less, 3 mg / kg (body weight) or less, 2.5 mg / kg (body weight) or less, 2 mg / kg (body weight) or less, 1.5 mg / kg (body weight) or less, or 1 mg / kg (body weight) or less.

[0038] In one embodiment, the composition may be a cosmetic composition.

[0039] The cosmetic composition according to an embodiment of the present invention may contain a cosmetically or dermatologically acceptable medium or matrix. As a dosage form suitable for topical application, it can be provided in, for example, as a solution, gel, solid, anhydrous paste, emulsion, suspension, microemulsion, microcapsule, microsphere, or ionic (liposome) and nonionic saccharin dispersion, or in the form of cream, lotion, emulsion, powder, ointment, spray, or concealer stick. These compositions can be prepared according to conventional methods in the art. The cosmetic composition may also be used in the form of a foam containing a compressed propellant aerosol composition.

[0040] The dosage form of the cosmetic composition is not particularly limited and can be appropriately selected according to the purpose. For example, it can be formulated into dosage forms such as lotion, toner, softening lotion, emulsion, milk lotion, moisturizing emulsion, nourishing emulsion, massage cream, nourishing cream, moisturizing cream, hand cream, foundation, serum, nourishing serum, face mask, soap, facial foam, facial cleanser, facial cream, makeup remover, powder, body lotion, moisturizing cream, moisturizing oil, body cleanser, and body essence.

[0041] When the dosage form of the cosmetic composition is a paste, cream, or gel, the carrier component may include animal fiber, plant fiber, wax, paraffin, starch, astragalus gum, cellulose derivatives, polyethylene glycol, silicone, bentonite, silica, talc, or zinc oxide, etc.

[0042] When the cosmetic composition is in the form of a powder or a spray, lactose, talc, silica, aluminum hydroxide, calcium silicate, or polyamide powder may be used as a carrier component. In particular, when the dosage form is a spray, it may further contain propellants such as chlorofluorocarbons, propane / butane, or dimethyl ether.

[0043] When the dosage form of the cosmetic composition is a solution or emulsion, a solvent, solvator or emulsifier is used as the carrier component, such as water, ethanol, isopropanol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propylene glycol, 1,3-butylethylene glycol oil, glycerol aliphatic ester, polyethylene glycol or fatty acid esters of sorbitol.

[0044] When the dosage form of the cosmetic composition is a suspension, liquid diluents such as water, ethanol or propylene glycol can be used as carrier components; suspending agents such as ethoxylated isostearyl alcohol, polyoxyethylene sorbitan ester and polyoxyethylene sorbitan anhydride ester; microcrystalline cellulose; aluminum hydroxide; bentonite, agar or tragacanth gum, etc.

[0045] When the dosage form of the cosmetic composition is a surfactant-containing cleanser, the carrier component may include fatty alcohol sulfates, fatty alcohol ether sulfates, sulfosuccinate monoesters, hydroxyethyl sulfonates, imidazoline derivatives, methyl taurate, sarcosinate, fatty acid amide ether sulfates, alkylamide betaine, fatty alcohols, fatty acid glycerides, fatty acid diethanolamides, vegetable oils, lanolin derivatives, or ethoxylated glycerol fatty acid esters, etc.

[0046] In addition to compound K, the cosmetic composition may also contain functional additives and ingredients included in general cosmetic compositions. As functional additives, they may include ingredients selected from the group consisting of water-soluble vitamins, oil-soluble vitamins, high-molecular-weight peptides, high-molecular-weight polysaccharides, sphingolipids, and seaweed extract.

[0047] In addition, the composition may also contain, as needed, ingredients commonly found in cosmetic compositions, along with the functional additives. Examples of such additional ingredients include oils, moisturizers, emollients, surfactants, organic and inorganic pigments, organic powders, UV absorbers, preservatives, bactericides, antioxidants, plant extracts, pH adjusters, ethanol, colorants, fragrances, blood circulation enhancers, cooling agents, antiperspirants, and purified water.

[0048] In one embodiment, the composition may be a non-therapeutic oral composition or a food composition.

[0049] The dosage form of the non-therapeutic oral composition or food composition is not particularly limited, and can be formulated as tablets, granules, pills, powders, liquid beverages, caramel, gels, strips, tea bags, etc. In addition to the active ingredient, those skilled in the art can easily select commonly used ingredients in the field according to the dosage form or intended use to formulate various dosage forms of non-therapeutic oral compositions or food compositions, which can produce synergistic effects when used simultaneously with other ingredients. The composition can be administered via various simple methods such as ingestion, drinking, injection, spraying, or squeezing.

[0050] In a non-therapeutic oral composition or food composition according to an embodiment of the present invention, the dosage or intake of the active ingredient can be determined at the level of a person skilled in the art and can vary depending on various factors such as the age, health status, and complications of the person receiving the medication or consuming it.

[0051] According to an embodiment of the present invention, a non-therapeutic oral composition or food composition may be, for example, various food products such as chewing gum, caramel products, candies, ice cream, and biscuits; beverage products such as soft drinks, mineral water, and alcoholic beverages; or oral products containing vitamins or minerals.

[0052] In addition to the above, a non-therapeutic oral composition or food composition according to an embodiment of the present invention may include various nutrients, vitamins, minerals (electrolytes), flavoring agents such as synthetic and natural flavoring agents, coloring agents and thickeners (cheese, chocolate, etc.), pectic acid and its salts, alginic acid and its salts, organic acids, protective colloidal thickeners, pH adjusters, stabilizers, preservatives, glycerin, alcohols, carbonating agents for use in carbonated beverages, etc. Furthermore, a non-therapeutic oral composition or food composition according to an embodiment of the present invention may include natural fruit juice and fruit pulp for making fruit juice beverages and vegetable beverages. These ingredients may be used alone or in combination. While the proportions of these additives are not critical, they typically range from 0 to 60 parts by weight per 100 parts by weight of the composition according to an embodiment.

[0053] As one embodiment, the present invention can be provided in the following forms.

[0054] A first embodiment may provide a composition containing compound K for improving the skin renewal cycle.

[0055] A second embodiment may provide a composition, according to the first embodiment, wherein the compound K contains an amount of 0.0002 to 0.04% by weight relative to the total weight of the composition.

[0056] A third embodiment may provide a composition in which, according to one or more of the first and second embodiments, the compound K increases the expression of p63.

[0057] The fourth embodiment may provide a composition in which, according to one or more of the first to third embodiments, the compound K increases the expression of KLF4.

[0058] The fifth embodiment may provide a composition, according to one or more of the first to fourth embodiments, wherein the compound K improves the skin renewal cycle in the epidermis.

[0059] The sixth embodiment may provide a composition, according to one or more of the first to fifth embodiments, wherein the compound K repairs the elongated skin renewal cycle in the epidermis.

[0060] The seventh embodiment may provide a composition wherein, according to one or more of the first to sixth embodiments, the daily dosage of said compound K is from 0.5 mg / kg (body weight) to 10 mg / kg (body weight).

[0061] The eighth embodiment may provide a composition according to one or more of the first to seventh embodiments, said composition being a cosmetic composition.

[0062] The ninth embodiment may provide a composition according to one or more of the first to eighth embodiments, wherein the composition is a non-therapeutic oral composition.

[0063] The present invention will now be described in more detail through experimental examples. However, these experimental examples are only for understanding the content of the present invention, and the scope of the present invention is not limited to these experimental examples. Modifications, substitutions, and insertions commonly known in the art can also be made, and these are also included within the scope of the present invention.

[0064] [Experimental Example 1] Skin Cytotoxicity Test

[0065] To confirm the cytotoxicity of compound K on human epidermal keratinocytes, 1 x 10⁻⁶ cells were used. 4 After seeding in 96-well plates, cells were cultured for 24 hours. Then, cells were treated with compound K to achieve final concentrations of 0.5 ppm, 1 ppm, 2 ppm, and 4 ppm per well, and cultured for 24 hours. Each well was then treated with 10 μl of Cell Counting Kit-8 (CCK-8) solution, cultured at 37°C for 2 hours, and absorbance was measured at 450 nm. Cell proliferation and toxicity were calculated as a percentage based on the absorbance of the control group. Figure 1 The result is shown in the figure.

[0066] from Figure 1 The results confirmed that compound K did not cause cytotoxicity at concentrations ranging from 0.5 ppm to 4 ppm.

[0067] [Experiment Example 2] Experiment on Accelerated Skin Aging

[0068] To confirm that external stimuli cause accelerated skin aging, human epidermal keratinocytes (HEMKs) were sampled at a concentration of 1 x 10⁻⁶. 4After seeding in 96-well plates, the culture was incubated for 24 hours. Then, IL-17A, an inflammatory senescence factor, was treated with the culture medium at a concentration of 50 μg / ml to induce an inflammatory response. After 24 hours, the culture medium was removed, replaced with PBS, and incubated at 20 mJ / cm². 2 Irradiation with ultraviolet light (UVB) or treatment of particulate matter (PM2.5) at 100 μg / ml or at 40 J / cm 2 After irradiation with blue light (HEV) and replacement of the culture medium with one containing 50 μg / ml of IL-17A, the cells were cultured for another 24 hours. Then, total RNA was extracted from skin keratinocytes using an RNA extraction kit (Qiagen, RNeasy Minikit), and cDNA was synthesized from the extracted RNA (Invitrogen, SuperScript VILO Master Mix). Changes in p63 and KLF4 expression levels were then observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probes (Applied Biosystems). Figure 2a and Figure 2b (Ultraviolet treatment) Figure 3a and Figure 3b (Dust treatment) Figure 4a and Figure 4b The result is shown in (Blue Light Processing).

[0069] from Figure 2a and Figure 2b The results confirmed that, compared with treatment with IL-17A alone or treatment with ultraviolet (UVB) alone, the expression of p63 and KLF4 was significantly reduced in the accelerated aging environment of UVB treatment after IL-17A treatment.

[0070] Similarly, from Figure 3a and Figure 3b , Figure 4a and Figure 4b The results confirmed that, compared with the cases of IL-17A treatment alone or treatment with only particulate matter (PM2.5) or blue light (HEV), the expression of p63 and KLF4 was significantly reduced in the accelerated aging environment of PM2.5 or HEV treatment after IL-17A treatment.

[0071] The experimental results above show that, on the basis of normal aging, the expression of p63 and KLF4 is significantly reduced in environments where aging is accelerated by external stimuli (ultraviolet rays, dust, blue light).

[0072] [Experiment Example 3] Confirmation Experiment on the Efficacy of Compound K at Various Concentrations on Skin Aging Caused by Ultraviolet Treatment

[0073] To confirm the efficacy of compound K at various concentrations on UV-treated aged skin, human epidermal keratinocytes were prepared at a concentration of 1 x 10⁻⁶. 4 After inoculating into 96-well plates and culturing for 24 hours, compound K was treated with concentrations of 0.5 ppm, 1 ppm, 2 ppm, and 4 ppm. After 30 hours, IL-17A was further treated with the culture medium at a concentration of 50 μg / ml. After 24 hours, the culture medium was removed and replaced with PBS, followed by inoculation with 20 mJ / cm². 2 Irradiated with ultraviolet (UVB) light and cultured for 24 hours. Then, total RNA was extracted from skin keratinocytes using an RNA extraction kit (Qiagen, RNeasy Mini kit), and cDNA was synthesized from the extracted RNA (Invitrogen, SuperScript VILO Master Mix). Changes in p63 and KLF4 expression levels were then observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probes (Applied Biosystems). The results are shown in Table 1 below.

[0074] Table 1

[0075]

[0076] The results in Table 1 confirm that when keratinocytes were pretreated with compound K at 1 ppm, 2 ppm, and 4 ppm, respectively, treatment with IL-17A and UVB to accelerate aging resulted in the recovery of decreased p63 and KLF4 expression. In particular, treatment at 2 ppm and 4 ppm showed significantly greater recovery of p63 expression compared to the positive control group EGCG, while the recovery of KLF4 expression was similar to that of the positive control group EGCG. The 2 ppm treatment showed the most significant recovery rate for both p63 and KLF4 expression.

[0077] [Experimental Example 4] Confirmation Experiment on the Efficacy of Compound K on Aging Skin Caused by Microdust Treatment

[0078] To confirm the efficacy of compound K on aging caused by particulate matter (PM2.5), human epidermal keratinocytes were used at a concentration of 1 x 10⁻⁶. 4 After seeding in 96-well plates and culturing for 24 hours, compound K was treated at a concentration of 2 ppm. After 30 minutes, IL-17A was further treated with the medium at a concentration of 50 μg / ml. After 24 hours, the culture medium was removed, replaced with PBS, and treated with 100 μg / ml PM2.5. The medium was then replaced with medium containing 50 μg / ml IL-17A and 2 ppm compound K, and cultured for another 24 hours. Total RNA was then extracted from skin keratinocytes using an RNA extraction kit (Qiagen, RNeasy Mini kit). cDNA was synthesized from the extracted RNA (Invitrogen, SuperScriptVILO Master Mix). Changes in p63 and KLF4 expression levels were observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probes (Applied Biosystems). As a positive control, 10 μM EGCG was used. The results are shown in Table 2 below.

[0079] Table 2

[0080]

[0081] The results in Table 2 confirm that when keratinocytes were pretreated with compound K at 2 ppm, and then treated with IL-17A and PM2.5 to induce accelerated skin aging, compound K significantly inhibited the reduction of p63 and KLF4 expression. Its effect was similar to or even more significant than that of EGCG as a positive control group.

[0082] [Experimental Example 5] Confirmation Experiment on the Efficacy of Compound K on Aging Skin Caused by Blue Light Treatment

[0083] To confirm the efficacy of compound K against blue light-induced aging (HEV), human epidermal keratinocytes were used at a concentration of 1 x 10⁻⁶. 4After inoculating into 96-well plates and culturing for 24 hours, compound K was treated at a concentration of 2 ppm. IL-17A was further treated with the medium at a concentration of 50 μg / ml after 30 minutes. After 24 hours, the culture medium was removed, replaced with PBS, and inoculated at 40 J / cm². 2 After irradiation with blue light (HEV), the culture medium was replaced with one containing 50 μg / ml of IL-17A and 2 ppm of compound K, and cultured for another 24 hours. Total RNA was then extracted from skin keratinocytes using an RNA extraction kit (Qiagen, RNeasy Mini kit), and cDNA was synthesized from the extracted RNA (Invitrogen, SuperScript VILOMaster Mix). Changes in p63 and KLF4 expression were then observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probes (Applied Biosystems). 10 μM EGCG was used as a positive control. The results are shown in Table 3 below.

[0084] Table 3

[0085]

[0086] The results in Table 3 confirm that when compound K was pretreated with 2 ppm to skin keratinocytes, and then IL-17A and HEV were treated to induce accelerated skin aging, compound K significantly inhibited the reduction of p63 and KLF4 expression. Its effect was similar to or even more significant than that of EGCG as a positive control group.

[0087] [Experiment Example 6] Confirmation Experiment on the Effect of Compound K on Cell Proliferation

[0088] To investigate the effects of compound K on cell proliferation under conditions that accelerate skin aging, human epidermal keratinocytes were used at a concentration of 1 x 10⁻⁶ cells / mL. 4 After seeding in 96-well plates, the culture was incubated for 24 hours. Then, IL-17A, an inflammatory senescence factor, was treated with the culture medium at a concentration of 50 μg / ml to induce an inflammatory response. After 24 hours, the culture medium was removed, replaced with PBS, and incubated at 20 mJ / cm². 2 Irradiation with ultraviolet light (UVB) or treatment of particulate matter (PM2.5) at 100 μg / ml or at 40 J / cm 2After irradiation with blue light (HEV), the culture medium was replaced with one containing 50 μg / ml IL-17A and 2 ppm compound K, and cultured for an additional 24 hours. Then, 10 μl of Cell Counting Kit-8 (CCK-8) solution was added to each well, and the cells were incubated at 37°C for 2 hours. The absorbance was then measured at 450 nm. Cell proliferation was calculated as a percentage of the absorbance of the control group, and the results are shown in Table 4 below.

[0089] Table 4

[0090]

[0091] As shown in Table 4, when inflammatory factors (IL-17A) and aging-accelerating factors (UVB, PM2.5, HEV) were treated in keratinocytes to induce accelerated skin aging, compound K significantly repaired reduced cell proliferation. The cell proliferation repair efficacy of compound K was also superior to that of EGCG, which served as a positive control group.

[0092] [Experimental Example 7] Confirmation Experiment on the Efficacy of Compound K on Artificial Skin Aging Caused by Ultraviolet Treatment

[0093] To confirm the efficacy of compound K against UV-induced aging of artificial skin, an artificial skin epidermal model (MatTek Life Science) was used to treat compound K in culture medium at a concentration of 2 ppm. After 30 minutes, IL-17A was further treated with the culture medium at a concentration of 100 μg / ml. After 24 hours, the culture medium was removed, replaced with PBS, and then treated with 100 mJ / cm². 2 After irradiation with ultraviolet light (UVB, Bio-Sun, Viber), the culture medium was replaced with one containing 100 μg / ml of IL-17A and 2 ppm of compound K, and cultured for an additional 48 hours. Then, paraffin blocks were prepared using artificial skin tissue, and Ki67, p63, and KLF4 were stained with antibodies (Abcam, NOVUS BIOLOGICALS) and their levels were measured. Ki67 is a representative marker of cell proliferation; restoration of decreased Ki67 expression indicates a return to normal cell proliferation function. Figures 5a to 5c The results are shown in the figures.

[0094] from Figures 5a to 5cThe results confirmed that when artificial skin epidermal tissue was pretreated with compound K, and then treated with IL-17A and UVB to accelerate aging, the reduced expression of Ki67, p63, and KLF4 was significantly restored. (Blue: DAPI (nuclear staining), green: KLF4).

[0095] The experimental results above show that, on the basis of normal aging, in an environment where aging is accelerated by external stimuli (ultraviolet rays, dust, blue light), compound K can effectively inhibit the reduction of Ki67, p63 and KLF4 expression. This indicates that compound K can enable keratinocytes to continuously self-replicate in the epidermis and continuously form keratin by promoting cell division, thereby effectively repairing the prolonged skin renewal cycle caused by the inhibition of epidermal cell proliferation.

[0096] [Dosage Form Example 1] Emulsion

[0097] Table 5

[0098]

[0099] [Dosage Form Example 2] Cream

[0100] Table 6

[0101]

[0102] [Dosage Form Example 3] Facial Mask

[0103] Table 7

[0104]

[0105] [Dosage Form Example 4] Toner

[0106] Table 8

[0107]

[0108] Specific portions of this specification have been described in detail above; however, it will be apparent to those skilled in the art that these specific descriptions are merely preferred embodiments, and the scope of this specification is not limited thereto. Therefore, the essential scope of this specification will be defined by the appended claims and their equivalents.

Claims

1. A composition containing compound K for improving the skin renewal cycle.

2. The composition according to claim 1, wherein, The compound K contains 0.0002 to 0.04% by weight relative to the total weight of the composition.

3. The composition according to claim 1, wherein, The compound K increases the expression of p63.

4. The composition according to claim 1, wherein, The compound K increases the expression of KLF4.

5. The composition according to claim 1, wherein, The compound K improves the skin renewal cycle in the epidermis.

6. The composition according to claim 1, wherein, The compound K repairs the prolonged skin renewal cycle in the epidermis.

7. The composition according to claim 1, wherein, The daily dosage of compound K is 0.5 mg / kg (body weight) to 10 mg / kg (body weight).

8. The composition according to any one of claims 1 to 7, wherein, The composition is a cosmetic composition.

9. The composition according to any one of claims 1 to 7, wherein, The composition is a non-therapeutic oral composition.

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