Composition for improving or increasing skin radiance or transparency containing compound k

Abstract

The present disclosure relates to a composition for improving or increasing skin radiance or transparency, containing compound K. Specifically, the composition for improving or increasing skin radiance or transparency, according to the present disclosure, improves barrier function by increasing KRT10 expression in the epidermal layer and at the same time, maintains stemness by recovering KLF4 expression, and suppresses collagen degradation by inhibiting MMP-1 expression in the dermal layer, and thus, by acting on both the epidermal layer and the dermal layer, can effectively reduce deterioration in skin radiance or transparency which is caused by uneven skin layers due to aging.

Description

Composition for improving or increasing skin radiance or transparency containing compound K

[0001] The present disclosure relates to a composition containing compound K for improving or increasing skin radiance or clarity.

[0002] Cross-reference to related applications

[0003] This application claims priority to Republic of Korea Patent Application No. 10-2024-0045897, filed April 4, 2024, the entire contents of which are incorporated herein by reference.

[0004] As skin tissue ages, inflammation increases, and external stimuli such as UVB rays, fine dust, and high-energy visible light (HVV) are known to induce skin aging. These external stimuli are believed to accelerate the natural aging process. Inflammatory aging and external stimuli damage the skin's barrier function and cause it to lose elasticity. This leads to uneven skin texture, which causes light to scatter instead of being reflected properly, resulting in a loss of radiance and clarity.

[0005] In addition, in order to improve skin radiance and transparency due to the smoothness of the skin surface, there is a limit to the effect of action only on the dermis layer, and it is necessary to effectively even out the skin surface through action on the epidermis layer.

[0006] [Prior Art Literature]

[0007] [Patent Document]

[0008] (Patent Document 1) Republic of Korea Patent Publication No. 10-2014-0003198

[0009] The present disclosure provides a composition that improves barrier function by increasing KRT10 expression in the epidermal layer, while simultaneously restoring KLF4 expression to maintain stem cell function, and inhibits collagen degradation by inhibiting MMP-1 expression in the dermal layer, thereby acting on both the epidermal layer and the dermal layer to effectively improve skin radiance or transparency reduction caused by uneven skin layers due to aging.

[0010] To achieve the above-mentioned purpose, one embodiment of the present invention provides a composition for improving or increasing skin radiance or transparency containing compound K.

[0011] The composition for improving or increasing skin radiance or transparency according to the present disclosure increases KRT10 expression in the epidermal layer to improve barrier function, while simultaneously restoring KLF4 expression to maintain stem cell function, and inhibits MMP-1 expression in the dermal layer to suppress collagen degradation, thereby acting on both the epidermal layer and the dermal layer to effectively improve skin radiance or transparency reduction caused by uneven skin layers due to aging.

[0012] Figure 1 shows the results of a skin cytotoxicity test of compound K.

[0013] Figures 2a to 2c show the results of confirming changes in the expression of KRT10, KLF4, and MMP-1 in an environment of accelerated skin aging caused by UVB treatment.

[0014] Figures 3a to 3c show the results of confirming changes in the expression of KRT10, KLF4, and MMP-1 in an environment of accelerated skin aging caused by fine dust (PM2.5) treatment.

[0015] Figures 4a to 4c show the results of confirming changes in the expression of KRT10, KLF4, and MMP-1 in an environment of accelerated skin aging caused by blue light (HEV) treatment.

[0016] Figures 5a to 5c show the results of confirming the efficacy of compound K on KRT10, KLF4, and MMP-1 in a skin accelerated aging environment caused by UVB treatment.

[0017] Figures 6a to 6c show the results of confirming the efficacy of compound K on KRT10, KLF4, and MMP-1 in an environment of accelerated skin aging caused by fine dust (PM2.5) treatment.

[0018] Figures 7a to 7c show the results of confirming the efficacy of compound K on KRT10, KLF4, and MMP-1 in a skin accelerated aging environment caused by blue light (HEV) treatment.

[0019] Figures 8a and 8b show the results of confirming the efficacy of compound K in restoring KRT10 (K10) and KLF4 expression on artificial skin subjected to accelerated aging by ultraviolet treatment.

[0020] Figures 9a and 9b show the results of confirming the efficacy of compound K in improving skin radiance or transparency on artificial skin subjected to accelerated aging by ultraviolet treatment.

[0021] Hereinafter, the present invention will be described in detail.

[0022] In one aspect, the present invention may relate to a composition for improving or increasing skin radiance or transparency, comprising compound K.

[0023] In one aspect, the present invention may relate to a method for improving or increasing skin radiance or clarity, comprising applying or administering an effective amount of compound K to a subject in need thereof.

[0024] In one aspect, the present invention may relate to the use of compound K for preparing a composition for improving or increasing skin radiance or clarity.

[0025] In one aspect, the present invention may relate to a compound K for use in improving or increasing skin radiance or clarity.

[0026] In one aspect, the present invention may relate to non-therapeutic uses of compound K for improving or increasing skin radiance or clarity.

[0027] Skin radiance or transparency is expressed by light reflection from the skin surface. The more uniform and smooth the skin surface and skin layer are, the more light is reflected without being scattered, which can increase skin radiance or transparency.

[0028] Specifically, skin radiance and transparency are determined by the reflection of light when it strikes the skin. When light strikes the skin surface, the light that is reflected directly determines the skin's radiance, while the light transmitted through the skin determines its transparency. Skin with high transparency is characterized by a large amount of light returning from within the skin when light of the same intensity is incident on the skin, and thus has a high degree of diffuse reflection. Skin radiance is significantly affected by the nature and condition of the skin's surface, and causes of reduced skin transparency include a decrease in gloss due to diffuse reflection on the skin's surface.

[0029] In one embodiment, the compound K may be represented by the following chemical formula 1.

[0030]

[0031] In one embodiment, the compound K may be contained in an amount of 0.0002 to 0.04 wt% relative to the total weight of the composition. Specifically, the compound K may be included in an amount of 0.0002 wt% or more, 0.0003 wt% or more, 0.0004 wt% or more, 0.0005 wt% or more, 0.0006 wt% or more, 0.0007 wt% or more, 0.0008 wt% or more, 0.0009 wt% or more, 0.001 wt% or more, 0.002 wt% or more, 0.003 wt% or more, 0.004 wt% or more, 0.005 wt% or more, 0.006 wt% or more, 0.007 wt% or more, 0.008 wt% or more, 0.009 wt% or more, 0.01 wt% or more, or 0.02 wt% or more, relative to the total weight of the composition, and further, the compound K may be included in an amount of 0.04 wt% or less, 0.03 wt% or less, relative to the total weight of the composition, It may be included in an amount of 0.02 wt% or less, 0.01 wt% or less, 0.009 wt% or less, 0.008 wt% or less, 0.007 wt% or less, 0.006 wt% or less, 0.005 wt% or less, 0.004 wt% or less, 0.003 wt% or less, 0.002 wt% or less, 0.001 wt% or less, 0.0009 wt% or less, 0.0008 wt% or less, 0.0007 wt% or less, 0.0006 wt% or less, 0.0005 wt% or less, 0.0004 wt% or less, or 0.0003 wt% or less.

[0032] In one embodiment, the compound K can increase the expression of KRT10. KRT10 is a biomarker associated with skin barrier function in the epidermal layer, and a decrease in the expression of KRT10 indicates that the skin barrier function in the epidermal layer is impaired.

[0033] In one embodiment, the compound K can improve barrier function in the epidermal layer by increasing the expression of KRT10.

[0034] In one embodiment, the compound K can increase the expression of KLF4. KLF4 is a biomarker associated with stem cell potential in the epidermal layer, and a decrease in the expression of KLF4 indicates a decrease in stem cell potential in the epidermal layer.

[0035] In one embodiment, the compound K can improve the stem cell capacity of skin keratinocytes in the epidermal layer by increasing the expression of KLF4.

[0036] In one embodiment, the compound K can inhibit the expression of MMP-1. MMP-1 is an enzyme that decomposes collagen present in the dermis, and an increase in the expression of MMP-1 indicates that the dermis has collapsed and elasticity has decreased.

[0037] In one embodiment, the compound K can effectively improve or increase skin radiance or transparency by acting on both the epidermal layer and the dermal layer by increasing the expression of at least one of KRT10 and KLF4 and inhibiting the expression of MMP-1, thereby making the skin layer uniform and smooth.

[0038] In one embodiment, the daily dose of the compound K may be 0.5 mg / kg body weight to 10 mg / kg body weight. Specifically, the daily application amount, application amount or intake amount of the compound K is 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, and further, the daily application amount of the compound K may be 10 mg / kg(body weight) or less, 9.5 mg / kg(body weight) or less, 9 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 May be less than mg / kg (body weight).

[0039] In one embodiment, the composition may be a cosmetic composition.

[0040] The cosmetic composition according to one embodiment of the present invention may contain a cosmetically or dermatologically acceptable medium or base. This may be provided in any formulation suitable for topical application, for example, in the form of a solution, gel, solid, anhydrous paste, an emulsion obtained by dispersing an oil phase in an aqueous phase, a suspension, a microemulsion, a microcapsule, a microgranule, or a vesicular dispersion of ionic (liposomes) and non-ionic types, or in the form of a cream, toner, lotion, powder, ointment, spray, or concealer stick. These compositions may be prepared according to methods conventional in the art. The cosmetic composition may also be used in the form of an aerosol composition further containing a propellant compressed in the form of a foam.

[0041] The above cosmetic composition is not particularly limited in its formulation and may be appropriately selected depending on the intended purpose. For example, it may be manufactured in the form of a skin lotion, skin softener, skin toner, lotion, milk lotion, moisture lotion, nutrition lotion, massage cream, nutrition cream, moisture cream, hand cream, foundation, essence, nutrition essence, pack, soap, cleansing foam, cleansing lotion, cleansing cream, cleansing water, powder, body lotion, body cream, body oil, body cleanser, and body essence.

[0042] When the formulation of the above cosmetic composition is a paste, cream or gel, animal fiber, plant fiber, wax, paraffin, starch, tragacanth, cellulose derivative, polyethylene glycol, silicone, bentonite, silica, talc or zinc oxide may be used as a carrier component.

[0043] When the formulation of the above cosmetic composition is a powder or spray, lactose, talc, silica, aluminum hydroxide, calcium silicate or polyamide powder may be used as a carrier component, and particularly in the case of a spray, a propellant such as chlorofluorohydrocarbon, propane / butane or dimethyl ether may be additionally included.

[0044] When the formulation of the above cosmetic composition is a solution or emulsion, a solvent, solvating agent or emulsifying agent is used as a carrier component, and examples thereof include water, ethanol, isopropanol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propylene glycol, 1,3-butylglycol oil, glycerol aliphatic ester, polyethylene glycol or fatty acid ester of sorbitan.

[0045] When the formulation of the above cosmetic composition is a suspension, a liquid diluent such as water, ethanol or propylene glycol, a suspending agent such as ethoxylated isostearyl alcohol, polyoxyethylene sorbitol ester and polyoxyethylene sorbitan ester, microcrystalline cellulose, aluminum metahydroxide, bentonite, agar or tragacanth, etc. can be used as a carrier component.

[0046] When the formulation of the above cosmetic composition is a surfactant-containing cleansing, aliphatic alcohol sulfate, aliphatic alcohol ether sulfate, sulfosuccinic acid monoester, isethionate, imidazolinium derivative, methyl taurate, sarcosinate, fatty acid amide ether sulfate, alkylamidobetaine, fatty alcohol, fatty acid glyceride, fatty acid diethanolamide, vegetable oil, linolenic derivative, or ethoxylated glycerol fatty acid ester may be used as a carrier component.

[0047] The above cosmetic composition may further include functional additives and ingredients included in general cosmetic compositions in addition to the above compound K. The functional additives 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 extracts.

[0048] In addition to the functional additives, the composition may also contain ingredients typically found in cosmetic compositions, as needed. Other ingredients to be included include, but are not limited to, oil-based ingredients, moisturizers, emollients, surfactants, organic and inorganic pigments, organic powders, ultraviolet absorbers, preservatives, bactericides, antioxidants, plant extracts, pH regulators, alcohols, pigments, fragrances, blood circulation promoters, cooling agents, antiperspirants, purified water, and the like.

[0049] In one embodiment, the composition may be a non-therapeutic oral composition or a food composition.

[0050] The dosage form of the above non-therapeutic oral composition or food composition is not particularly limited, but may be formulated as, for example, tablets, granules, pills, powders, liquids such as drinks, caramels, gels, bars, tea bags, etc. In addition to the active ingredient, the non-therapeutic oral composition or food composition of each dosage form can be appropriately selected and combined by a person skilled in the art according to the dosage form or purpose of use by appropriately selecting the ingredients commonly used in the relevant field, and a synergistic effect may occur when applied simultaneously with other raw materials. The above composition can be administered in various ways such as simple ingestion, drinking, injection administration, spray administration, or squeeze administration.

[0051] In a non-therapeutic oral composition or food composition according to one embodiment of the present invention, the determination of the dosage or intake amount of the active ingredient is within the level of a person skilled in the art, and may vary depending on various factors such as the age, health condition, and complications of the subject to be administered or consumed.

[0052] A non-therapeutic oral composition or food composition according to one embodiment of the present invention may be, for example, various food products such as chewing gum, caramel products, candy, ice cream, and confectionery, beverage products such as soft drinks, mineral water, and alcoholic beverages, and oral products containing vitamins or minerals.

[0053] In addition to the above, the non-therapeutic oral composition or food composition according to one embodiment of the present invention may include various nutrients, vitamins, minerals (electrolytes), flavoring agents such as synthetic flavoring agents and natural flavoring agents, coloring agents and enhancers (cheese, chocolate, etc.), pectic acid and its salts, alginic acid and its salts, organic acids, protective colloid thickeners, pH adjusters, stabilizers, preservatives, glycerin, alcohol, carbonating agents used in carbonated beverages, etc. In addition, the non-therapeutic oral composition or food composition according to one embodiment of the present invention may include fruit pulp for the production of natural fruit juice and fruit juice drinks and vegetable drinks. These components may be used independently or in combination. The proportion of these additives is not so critical, but is typically included in the range of 0 to about 60 parts by weight per 100 parts by weight of the composition according to one embodiment of the present invention.

[0054]

[0055] The present invention may provide, as an example, the following embodiments.

[0056] The first embodiment can provide a composition for improving or increasing skin radiance or transparency, containing compound K.

[0057] A second embodiment can provide a composition in which, in the first embodiment, the compound K is contained in an amount of 0.0002 to 0.04 wt% based on the total weight of the composition.

[0058] A third embodiment can provide a composition according to at least one of the first embodiment and the second embodiment, wherein the compound K increases the expression of KRT10.

[0059] A fourth embodiment can provide a composition according to one or more of the first to third embodiments, wherein the compound K increases the expression of KLF4.

[0060] The fifth embodiment can provide a composition according to one or more of the first to fourth embodiments, wherein the compound K inhibits the expression of MMP-1.

[0061] A sixth embodiment can provide a composition according to one or more of the first to fifth embodiments, wherein the compound K improves a barrier function in the epidermal layer.

[0062] The seventh embodiment can provide a composition according to at least one of the first to sixth embodiments, wherein the compound K improves the stem cell capacity of skin keratinocytes in the epidermal layer.

[0063] The eighth embodiment can provide a composition according to at least one of the first to seventh embodiments, wherein the daily application amount of the compound K is 0.5 mg / kg (body weight) to 10 mg / kg (body weight).

[0064] The ninth embodiment can provide a composition that is a cosmetic composition according to one or more of the first to eighth embodiments.

[0065] The tenth embodiment can provide a composition that is a non-therapeutic oral composition according to one or more of the first to ninth embodiments.

[0066]

[0067] Hereinafter, the present invention will be described in more detail through experimental examples. However, these experimental examples are provided merely to facilitate understanding 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 may be performed, and such modifications are also included within the scope of the present invention.

[0068]

[0069] [Experimental Example 1] Skin Cell Toxicity Experiment

[0070] To determine the cytotoxicity of compound K on human epidermal keratinocytes, 1x10 human epidermal keratinocytes were seeded in a 96-well plate. 4 After seeding, the cells were cultured for 24 hours. After that, the cells were treated with the final concentration of Compound K per well of 0.5 ppm, 1 ppm, 2 ppm, and 4 ppm, respectively, and cultured for 24 hours. 10 μl Cell Counting Kit-8 (CCK-8) solution was treated to each well and cultured at 37°C for 2 hours, and the absorbance was measured at 450 nm. The cell proliferation and toxicity effects were calculated as a percentage based on the absorbance of the control group. The results are shown in Fig. 1.

[0071] From the results in Fig. 1, it was confirmed that compound K did not cause cytotoxicity at concentrations of 0.5 ppm to 4 ppm.

[0072]

[0073] [Experimental Example 2] Experiment on Accelerated Skin Aging

[0074] To confirm the acceleration of skin aging due to external stimuli, human epidermal keratinocytes were seeded at 1x10 in a 96-well plate. 4After seeding, the cells were cultured for 24 hours. Afterwards, an inflammatory response was induced by treating the medium with IL-17A, an inflammatory aging factor, at a concentration of 50 μg / ml. After 24 hours, the culture medium was removed and replaced with PBS, and then exposed to ultraviolet (UVB) light at 20 mJ / cm 2 Investigate or treat 100μg / ml of fine dust (PM2.5) or 40 J / cm of blue light (HEV) 2 , and cultured for an additional 24 hours after replacing the medium with IL-17A at a concentration of 50 μg / ml. After that, total RNA was extracted from skin keratinocytes using an RNA extraction kit (Quiagen, RNease Mini kit), and cDNA was synthesized from the extracted RNA (Invitrogen, SuperScript VILO Master Mix). Then, the expression levels of KRT10, KLF4, and MMP-1 were observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probe (Applied Biosystems). The results are shown in Figs. 2a to 2c (ultraviolet treatment), 3a to 3c (fine dust treatment), and 4a to 4c (blue light treatment).

[0075] From the results of Figures 2a to 2c, it was confirmed that the expression of KRT10 and KLF4 was significantly reduced and the expression of MMP-1 was significantly increased in an accelerated aging environment treated with UVB after IL-17A treatment, compared to when only IL-17A was treated or only ultraviolet rays (UVB) were treated.

[0076] Similarly, from the results of FIGS. 3a to 3c and 4a to 4c, it was confirmed that the expression of KRT10 and KLF4 was significantly reduced and the expression of MMP-1 was significantly increased in an accelerated aging environment where PM2.5 or HEV was treated after IL-17A treatment, compared to when only IL-17A was treated or only fine dust (PM2.5) or blue light (HEV) was treated.

[0077] From the above experimental results, it was found that in an environment where aging was accelerated by external stimuli (ultraviolet rays, fine dust, blue light) in addition to general aging, the expression of KRT10 and KLF4 decreased more significantly and the expression of MMP-1 increased more significantly.

[0078] Epidermolytic hyperkeratosis is a genetic disorder caused by mutations in KRT10, which results in the inability to express it. This condition causes thick, dark, scaly skin and makes it brittle. Specifically, KRT10 plays a crucial role in skin barrier function through keratin formation, smoothing the skin surface. Therefore, restoring KRT10 expression, which decreases with age, smooths the skin surface and increases radiance and clarity.

[0079] Keratinocyte stem cells are responsible for the self-division of keratinocytes. They ensure the continued production of keratinocytes and play a crucial role in determining the formation and shedding of keratin. As we age, the stem cell capacity of keratinocytes declines, leading to phenomena such as increased keratin size and decreased shedding rates, which in turn affect the roughness of the skin surface. Therefore, restoring the expression of KLF4, a gene responsible for stem cell capacity, normalizes stem cell capacity and keratin formation, thereby increasing the uniformity of the skin surface.

[0080] MMP-1 is an enzyme that breaks down collagen proteins. Collagen proteins are present in the dermis, and their degradation damages the dermal ECM structure, causing wrinkles. Therefore, suppressing MMP-1 expression inhibits collagen protein degradation, strengthening the dermal structure and preventing the loss of skin clarity that can occur due to decreased skin elasticity.

[0081]

[0082] [Experimental Example 3] Experiment to confirm the efficacy of compound K at different concentrations on aging skin caused by UV treatment.

[0083] To determine the efficacy of compound K at different concentrations on aged skin caused by UV treatment, human epidermal keratinocytes were seeded in a 96-well plate at a density of 1x10 4 After seeding, the cells were cultured for 24 hours and then treated with compound K at concentrations of 0.5 ppm, 1 ppm, 2 ppm, and 4 ppm. After 30 minutes, IL-17A was additionally treated to the medium at a concentration of 50 μg / ml. After 24 hours, the culture medium was removed, replaced with PBS, and exposed to ultraviolet (UVB) light at 20 mJ / cm 2 and cultured for 24 hours. Afterwards, total RNA was extracted from skin keratinocytes using an RNA extraction kit (Quiagen, RNease Mini kit), and cDNA was synthesized from the extracted RNA (Invitrogen, SuperScript VILO Master Mix). Then, the change in KRT10 expression level was observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probe (Applied Biosystems). The results are shown in Table 1 below.

[0084] Stimulus treatment concentration KRT10 expression level (Fold) Control (untreated) - (unstimulated) - 1 Control (untreated) IL-17A + UVB - 0.14 Compound K 0.5 ppm 0.191 ppm 0.182 ppm 0.5 14 ppm 0.47 EGCG 10 μM 0.40

[0085] From the results in Table 1, it was confirmed that when skin keratinocytes were pretreated with 0.5 ppm, 1 ppm, 2 ppm, and 4 ppm of compound K, and then treated with IL-17A and UVB to accelerate aging, the reduced expression of KRT10 was restored. In particular, when treated with 2 ppm and 4 ppm, the effect of restoring KRT10 expression was superior to that of the positive control, EGCG, and among them, the expression restoration rate of KRT10 was the best when treated with 2 ppm.

[0086]

[0087] [Experimental Example 4] Experiment to Confirm the Efficacy of Compound K on Aged Skin by Stimulus

[0088] To confirm the inhibitory effect of compound K on accelerated aging caused by ultraviolet (UVB), fine dust (PM2.5), and blue light (HEV), human epidermal keratinocytes were seeded in a 96-well plate at a density of 1x10 4 After seeding, the cells were cultured for 24 hours and then treated with compound K at a concentration of 2 ppm. After 30 minutes, IL-17A was additionally treated to the medium at a concentration of 50 μg / ml. After 24 hours, the culture medium was removed and replaced with PBS, and then exposed to ultraviolet (UVB) light at 20 mJ / cm 2 Investigate or treat 100μg / ml of fine dust (PM2.5) or 40 J / cm of blue light (HEV) 2, and the medium was replaced with a medium containing 50 μg / ml of IL-17A and 2 ppm of compound K, and then cultured for an additional 24 hours. Afterwards, total RNA was extracted from skin keratinocytes using an RNA extraction kit (Quiagen, RNease Mini kit), and cDNA was synthesized (Invitrogen, SuperScript VILO Master Mix) from the extracted RNA, and then the expression levels of KRT10, KLF4, and MMP-1 were observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and a Taqman probe (Applied Biosystems). 10 μM EGCG was used as a positive control. The results are shown in Figs. 5a to 5c (ultraviolet treatment), 6a to 6c (fine dust treatment), and 7a to 7c (blue light treatment).

[0089] From the results of FIGS. 5a to 5c, when skin keratinocytes were pretreated with 2 ppm of compound K and then treated with IL-17A and UVB to induce accelerated skin aging, it was confirmed that compound K significantly suppressed the decrease in expression of KRT10 and KLF4 and the increase in expression of MMP-1, which was similar to or even superior to the effect of EGCG, the positive control.

[0090] Similarly, from the results of FIGS. 6a to 6c and FIGS. 7a to 7c, when skin keratinocytes were pretreated with 2 ppm of compound K and then treated with IL-17A and PM2.5 or HEV to induce accelerated skin aging, it was confirmed that compound K significantly suppressed the decrease in the expression of KRT10 and KLF4 and the increase in the expression of MMP-1, which was similar to or even superior to the effect of EGCG, the positive control.

[0091]

[0092] [Experimental Example 5] Experiment to Confirm the Efficacy of Compound K on Artificial Skin Aged by UV Treatment

[0093] To confirm the efficacy of compound K on aging artificial skin by UV treatment, compound K was treated in the medium at a concentration of 2 ppm in an artificial skin epidermal model (MatTek Life Science). After 30 minutes, IL-17A was additionally treated in the medium at a concentration of 100 μg / ml. After 24 hours, the culture medium was removed and replaced with PBS, and then exposed to UV light (UVB, Bio-Sun, Viber) at 100 mJ / cm 2 After examining, the medium was changed to one containing IL-17A at a concentration of 100 μg / ml and compound K at a concentration of 2 ppm, and then cultured for an additional 28 hours. Afterwards, paraffin blocks were made using artificial skin tissue, and the amounts of KRT10 (K10) and KLF4 were measured by staining them with antibodies (Covance, NOVUS BIOLOGICALS), and the results are shown in Fig. 8a and Fig. 8b, respectively. (Blue: DAPI (nuclear stain), green: KLF4).

[0094] From the results of FIGS. 8a and 8b, it was confirmed that when the artificial skin epidermal tissue was pretreated with compound K and then treated with IL-17A and UVB to accelerate aging, the reduced expression of KRT10 and KLF4 was significantly restored.

[0095]

[0096] [Experimental Example 6] Experiment to confirm the efficacy of Compound K in improving skin radiance or transparency on artificial skin aged by UV treatment.

[0097] To determine the efficacy of Compound K in improving skin radiance and transparency on aging artificial skin, skin radiance and transparency were captured using VISIA-CR (Canfield Imaging Systems, USA) and analyzed using Image-pro plus (Media Cybernetics, USA). Specifically, skin radiance was measured by measuring the light reflected directly from the skin, not the light scattered from the skin. Skin transparency was analyzed by measuring the amount of light scattered within the skin using an RGB light source. The results are shown in Figures 9a and 9b.

[0098] From the results of FIGS. 9a and 9b, it was confirmed that when the artificial skin epidermal tissue was pretreated with compound K and then treated with IL-17A and UVB to accelerate aging, the decreased radiance or transparency was restored.

[0099]

[0100] From the above experimental results, it was found that Compound K effectively suppressed the decrease in expression of KRT10 and KLF4 and the increase in expression of MMP-1 in an environment where aging was accelerated by external stimuli (ultraviolet rays, fine dust, blue light) in addition to general aging. Through this, it was found that Compound K can act on the barrier function and stem cell function in the epidermis as well as the dermis layer of the skin, making the skin layer even and smooth and effectively improving skin radiance or transparency.

[0101]

[0102] [Formulation Example 1] Lotion

[0103] Ingredients (weight) Compound K 0.03 L-ascorbic acid-2-magnesium phosphate 1.00 Soluble collagen (1% aqueous solution) 1.00 Sodium citrate 0.10 Citric acid 0.05 Licorice extract 0.20 1,3-butylene glycol 3.00 Remaining tablet amount

[0104] [Formulation Example 2] Cream

[0105] Ingredient content (weight) Compound K0.03 Polyethylene glycol monostearate 2.00 Glycerin 5.00 Cetyl alcohol 4.00 Squalene 4.00 Liquid paraffin 10.00 Tris-2-ethylhexane glyceryl 6.00 Sphingoglycolipid 1.00 1,3-butylene glycol 7.00 Remaining tablet amount

[0106] [Formulation Example 3] Pack

[0107] Ingredients (weight) Compound K0.03 Polyvinyl alcohol 13.00 L-ascorbic acid-2-phosphate magnesium salt 1.00 Lauroyl hydroxyproline 1.00 Water-soluble collagen (1% aqueous solution) 2.00 1,3-butylene glycol 3.00 Ethanol 5.00 Remaining tablet amount

[0108] [Formulation Example 4] Toner

[0109] Ingredient content (weight) Compound K 0.03 Glycerin 3.0 Butylene glycol 2.0 Propylene glycol 2.0 Carboxyvinyl polymer 0.1 PEG-12 Nonylphenyl ether 0.2 Polysorbate-80 0.4 Ethanol 10.0 Triethanolamine 0.1 Preservative, colorant, fragrance Appropriate amount of purified water remaining

[0110] While specific portions of this specification have been described in detail above, it should be apparent to those skilled in the art that these specific descriptions are merely preferred implementation examples and do not limit the scope of this specification. Therefore, the substantial scope of this specification is defined by the appended claims and their equivalents.

Claims

1. A composition containing compound K for improving or increasing skin radiance or transparency.

2. In paragraph 1, A composition wherein the compound K is contained in an amount of 0.0002 to 0.04 wt% based on the total weight of the composition.

3. In paragraph 1, The above compound K is a composition that increases the expression of KRT10.

4. In paragraph 1, The above compound K is a composition that increases the expression of KLF4.

5. In paragraph 1, The above compound K is a composition that inhibits the expression of MMP-1.

6. In paragraph 1, The above compound K is a composition that improves the barrier function in the epidermal layer.

7. In paragraph 1, The above compound K is a composition that improves the stem cell capacity of skin keratinocytes in the epidermal layer.

8. In paragraph 1, A composition wherein the daily application amount of the compound K is 0.5 mg / kg (body weight) to 10 mg / kg (body weight).

9. In any one of paragraphs 1 to 8, A composition, which is a cosmetic composition.

10. In any one of paragraphs 1 to 8, A composition which is a non-therapeutic oral composition.

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