Composition for reducing skin sagging containing compound k

Abstract

The present disclosure relates to a composition for reducing skin sagging, containing compound K. Specifically, the composition for reducing skin sagging, according to the present disclosure, strengthens dermoepidermal junction (DEJ) function by increasing the expression of Col7A1 and Col17A1, which are proteins constituting the DEJ that connects the epidermal layer and the dermal layer, thereby improving the binding strength between the epidermal layer and the dermal layer and tightening the junction therebetween, and thus can effectively reduce skin sagging caused by damage to the DEJ function due to aging.

Description

Composition for improving skin sagging containing compound K

[0001] The present disclosure relates to a composition for improving skin sagging containing compound K.

[0002] Cross-reference to related applications

[0003] This application claims priority to Republic of Korea Patent Application No. 10-2024-0045899, filed April 4, 2024, the entire contents of which are incorporated herein by reference.

[0004] As skin tissue ages, its inflammatory response increases, and external stimuli such as UVB rays, fine dust, and high-energy visible light (high-energy visible light) are known to induce skin aging. These external stimuli are believed to accelerate the natural aging processes. Inflammatory aging and external stimuli damage the skin's barrier function and cause a loss of elasticity. In particular, damage to the dermoepidermal junction (DEJ), which connects the epidermis and dermis, exacerbates skin sagging.

[0005] Therefore, in order to improve skin sagging, it is necessary to increase the stability of the skin layer by strengthening the bond between the dermis and epidermis layers.

[0006] [Prior Art Literature]

[0007] [Patent Document]

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

[0009] The present disclosure aims to provide a composition that effectively improves skin sagging caused by damage to DEJ function due to aging by increasing the expression of Col7A1 and Col17A1, which are proteins constituting DEJ (dermoepidermal junction) connecting the epidermis and dermis, thereby enhancing DEJ function and strengthening the bonding strength between the epidermis and dermis, thereby strengthening the boundary between the epidermis and dermis.

[0010] In order to achieve the above-mentioned purpose, one embodiment of the present invention provides a composition for improving skin sagging containing compound K.

[0011] The composition for improving skin sagging according to the present disclosure can effectively improve skin sagging caused by damage to DEJ function due to aging by increasing the expression of Col7A1 and Col17A1, which are proteins constituting DEJ (dermoepidermal junction) connecting the epidermal layer and the dermal layer, thereby enhancing DEJ function and strengthening the bonding strength between the epidermal layer and the dermal layer and solidifying the boundary between the epidermal layer and the dermal layer.

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

[0013] Figures 2a and 2b show the results of confirming changes in the expression of Col7A1 and Col17A1 in an environment of accelerated skin aging caused by UVB treatment.

[0014] Figures 3a and 3b show the results of confirming changes in the expression of Col7A1 and Col17A1 in an environment of accelerated skin aging caused by fine dust (PM2.5) treatment.

[0015] Figures 4a and 4b show the results of confirming changes in the expression of Col7A1 and Col17A1 in an environment of accelerated skin aging caused by blue light (HEV) treatment.

[0016] Figure 5 shows the results of confirming the efficacy of compound K against accelerated skin aging caused by UVB treatment on artificial skin.

[0017] Hereinafter, the present invention will be described in detail.

[0018] In one aspect, the present invention may relate to a composition for improving skin sagging containing compound K.

[0019] In one aspect, the present invention may relate to a method for improving sagging skin, comprising applying or administering an effective amount of compound K to a subject in need thereof.

[0020] In one aspect, the present invention may relate to the use of compound K for preparing a composition for improving skin sagging.

[0021] In one aspect, the present invention may relate to a compound K for use in improving skin sagging.

[0022] In one aspect, the present invention may relate to non-therapeutic uses of compound K for improving skin sagging.

[0023] Sagging skin is affected by gravity. It can be prevented or improved only when epidermal cells forming the epidermis are tightly packed and the epidermis and dermis are firmly connected. Elasticity, on the other hand, is related to the skin's resilience and is linked to collagen in the dermis. Thus, sagging skin, which is directly related to the function of the epidermal-dermal junction (DEJ), is distinct from elasticity.

[0024] While sagging skin and elasticity are both properties associated with aging, their definitions and mechanisms differ. Sagging skin primarily refers to the downward sagging of skin tissue due to gravity. As we age, the supporting structures of the skin weaken, making the skin appear even more saggy.

[0025] Skin elasticity refers to the skin's ability to return to its original shape after being stretched. This property is closely related to the quality and quantity of collagen and elastin fibers. When elasticity is reduced, the skin can easily stretch without any obvious stimulus, leading to wrinkles and sagging. In other words, reduced skin elasticity makes sagging more likely. However, sagging skin can be caused by a combination of factors, including changes in the skin's microstructure, loss of fat tissue beneath the skin, and changes in elasticity.

[0026] The dermoepidermal junction (DEJ) is the connection between the epidermis and dermis, and plays a crucial role in the structural integrity and function of the skin. The DEJ provides support to the epidermis and facilitates the transport of nutrients and metabolites between the dermis and epidermis. Structural changes in the DEJ can significantly impact the appearance and severity of skin sagging. The DEJ contains specialized structural proteins, such as COL7 and COL17, which contribute to its structural integrity. Aging-related decline in DEJ structural proteins weakens skin tension and increases skin sagging. The DEJ structure is not flat but curved, a structure called the rete ridge. Rete ridges increase the contact area between the epidermis and dermis, distribute the physical load applied to the epidermis, and contribute to the attachment of the epidermal and dermal layers. Rete ridges flatten with age, and this structural change in the rete ridge leads to a decrease in the bonding strength between the epidermis and dermis, which in turn causes skin sagging. Furthermore, changes in the expression of DEJ-specific structural proteins have been reported to alter the Rete ridge structure, and increased expression of specific collagen proteins present in the DEJ has been reported to improve skin sagging.

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

[0028]

[0029] 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.

[0030] In one embodiment, the compound K can increase the expression of Col7A1.

[0031] In one embodiment, the compound K can increase the expression of Col17A1.

[0032] Col7A1 and Col17A1 are proteins that constitute the DEJ (dermoepidermal junction), and a decrease in Col7A1 and Col17A1 damages the function of the DEJ, which holds epidermal cells firmly and strengthens the bond between the epidermal layer and the dermal layer, causing skin sagging.

[0033] In one embodiment, the compound K can enhance DEJ (epidermal-dermal junction) function.

[0034] In one embodiment, the compound K can improve the bonding strength between the epidermal layer and the dermal layer.

[0035] In one embodiment, the compound K can enhance DEJ (epidermal dermal junction) function by increasing the expression of one or more of Col7A1 and Col17A1.

[0036] In one embodiment, the compound K can enhance the bonding between the epidermal layer and the dermal layer by increasing the expression of one or more of Col7A1 and Col17A1.

[0037] In one embodiment, the compound K can improve skin sagging by increasing the expression of at least one of Col7A1 and Col17A1, thereby enhancing DEJ (epidermal dermal junction) function, thereby improving the bonding strength between the epidermal layer and the dermal layer, and strengthening the boundary between the epidermal layer and the dermal layer.

[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 skin sagging 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 Col7A1.

[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 Col17A1.

[0060] The fifth embodiment can provide a composition according to at least one of the first to fourth embodiments, wherein the compound K improves DEJ (dermodpidermal junction) function.

[0061] The sixth embodiment can provide a composition in which, in one or more of the first to fifth embodiments, the compound K improves the bonding strength between the epidermal layer and the dermal layer.

[0062] The seventh embodiment can provide a composition according to at least one of the first to sixth embodiments, wherein the daily application amount of the compound K is 0.5 mg / kg (body weight) to 10 mg / kg (body weight).

[0063] The eighth embodiment can provide a composition that is a cosmetic composition according to one or more of the first to seventh embodiments.

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

[0065]

[0066] 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.

[0067]

[0068] [Experimental Example 1] Skin Cell Toxicity Experiment

[0069] 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.

[0070] 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.

[0071]

[0072] [Experimental Example 2] Experiment to accelerate skin aging

[0073] 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 Col7A1 and Col17A1 were observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and a Taqman probe (Applied Biosystems). The results are shown in Figs. 2a and 2b (ultraviolet treatment), 3a and 3b (fine dust treatment), and 4a and 4b (blue light treatment).

[0074] From the results of Figures 2a and 2b, it was confirmed that the expression of Col7A1 and Col17A1 was significantly reduced 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.

[0075] Similarly, from the results of FIGS. 3a and 3b, and 4a and 4b, it was confirmed that the expression of Col7A1 and Col17A1 was significantly reduced 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.

[0076] From the above experimental results, it was found that the expression of Col7A1 and Col17A1 was reduced more significantly in an environment where aging was accelerated by external stimuli (ultraviolet rays, fine dust, blue light) in addition to general aging.

[0077] Decreased Col7A1 and Col17A1 expression is known to weaken the DEJ structure and alter the rete ridge structure, accelerating skin aging. Therefore, restoring reduced Col7A1 and Col17A1 expression may prevent and improve DEJ and rete ridge structural alterations, thereby preventing and improving skin sagging.

[0078]

[0079] [Experimental Example 3] Experiment to confirm the efficacy of compound K at different concentrations on aging skin caused by UV treatment.

[0080] 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 2and 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 expression levels of Col7A1 and Col17A1 were 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.

[0081] Stimulus treatment concentration Col7A1 expression level (Fold) Col17A1 expression level (Fold) Control (untreated) - (unstimulated) - 11 Control (untreated) IL-17A + UVB - 0.32 0.39 Compound K 0.5 ppm 0.32 0.40 1 ppm 0.34 0.45 2 ppm 1.39 1.174 ppm 1.21 1.09 EGCG 10 μM 0.38 0.66

[0082] From the results in Table 1, it was confirmed that when skin keratinocytes were pretreated with 1 ppm, 2 ppm, and 4 ppm of compound K, respectively, and then treated with IL-17A and UVB to accelerate aging, the reduced expression of Col7A1 and Col17A1 was restored. In particular, when treated with 2 ppm and 4 ppm, the effect of restoring Col7A1 and Col17A1 expression was significantly superior to that of the positive control, EGCG, and among them, it was confirmed that the expression restoration rate of Col7A1 and Col17A1 was the best when treated with 2 ppm.

[0083]

[0084] [Experimental Example 4] Experiment to Confirm the Efficacy of Compound K on Aged Skin Treated with Fine Dust

[0085] To confirm the efficacy of compound K against aging caused by fine dust (PM2.5), 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, and after 24 hours, the culture medium was removed and replaced with PBS, and then 100 μg / ml of fine dust (PM2.5) was treated, and the medium was replaced with IL-17A at a concentration of 50 μg / ml and compound K at a concentration of 2 ppm, and then cultured for an additional 24 hours. 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), and then the expression levels of Col7A1 and Col17A1 were observed using a 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probe (Applied Biosystems). 10 μM EGCG was used as a positive control. The results are shown in Table 2 below.

[0086] Stimulated Col7A1 expression level (Fold) Col17A1 expression level (Fold) Control group (untreated) - (unstimulated) 11 Control group (untreated) IL-17A + PM2.5 0.4 2 0.6 1 Compound K 0.6 4 0.8 0 EGCG 0.7 1 0.73

[0087] From the results in Table 2, when skin keratinocytes were pretreated with 2 ppm of compound K and then treated with IL-17A and PM2.5 to induce accelerated skin aging, it was confirmed that compound K significantly suppressed the decrease in the expression of Col7A1 and Col17A1, and this effect was similar to or even superior to that of EGCG, the positive control.

[0088]

[0089] [Experimental Example 5] Experiment to Confirm the Efficacy of Compound K on Aged Skin Treated with Blue Light

[0090] To determine the efficacy of compound K against blue light (HEV)-induced aging, 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 blue light (HEV) at 40 J / cm. 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 from the extracted RNA (Invitrogen, SuperScript VILO Master Mix), followed by 7500 Fast Real-time PCR System (Thermo Fisher Scientific) and Taqman probe (Applied Biosystems) to observe the changes in the expression levels of Col7A1 and Col17A1. 10 μM EGCG was used as a positive control. The results are shown in Table 3 below.

[0091] Stimulated Col7A1 expression level (Fold) Col17A1 expression level (Fold) Control group (untreated) - (unstimulated) 11 Control group (untreated) IL-17A + HEV 0.39 0.73 Compound K 0.58 0.90 EGCG 0.62 0.89

[0092] From the results in Table 3, when skin keratinocytes were pretreated with 2 ppm of compound K and then treated with IL-17A and HEV to induce accelerated skin aging, it was confirmed that compound K significantly suppressed the decrease in the expression of Col7A1 and Col17A1, and this effect was similar to or even superior to that of EGCG, the positive control.

[0093]

[0094] [Experimental Example 6] Experiment to Confirm the Efficacy of Compound K on Artificial Skin Aged by UV Treatment

[0095] 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 100 μg / ml of IL-17A and 2 ppm of compound K, and then cultured for an additional 48 hours. Afterwards, paraffin blocks were made using artificial skin tissue, and Col17A1 was stained with antibody (Abcam) and the amount was measured. The results are shown in Fig. 5 (blue: DAPI (nuclear stain), green: Col17A1).

[0096] From the results in Fig. 5, 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 Col17A1 was significantly restored.

[0097]

[0098] From the above experimental results, it was found that Compound K effectively suppressed the decrease in the expression of Col7A1 and Col17A1 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 effectively improve skin sagging caused by damage to DEJ function due to aging by enhancing DEJ (epidermal junction) function, improving the bonding strength between the epidermis and dermis, and solidifying the boundary between the epidermis and dermis.

[0099]

[0100] [Formulation Example 1] Lotion

[0101] 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

[0102] [Formulation Example 2] Cream

[0103] 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

[0104] [Formulation Example 3] Pack

[0105] 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

[0106] [Formulation Example 4] Toner

[0107] 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

[0108]

[0109] 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 for improving skin sagging containing compound K.

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 Col7A1.

4. In paragraph 1, The above compound K is a composition that increases the expression of Col17A1.

5. In paragraph 1, The above compound K is a composition that strengthens the DEJ (dermodpidermal junction) function.

6. In paragraph 1, The above compound K is a composition that improves the bonding strength between the epidermal layer and the dermal layer.

7. 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).

8. In any one of paragraphs 1 to 7, A composition, which is a cosmetic composition.

9. In any one of paragraphs 1 to 7, A composition which is a non-therapeutic oral composition.

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