Cosmetic composition for skin improvement containing ginsenosides

Abstract

The present disclosure relates to a cosmetic composition for skin improvement containing ginsenoside. The cosmetic composition for alleviating skin wrinkles or improving skin elasticity according to the present disclosure significantly increases biosynthesis of collagen and hyaluronic acid in the skin, thereby exhibiting effects of inhibiting wrinkle formation and improving skin elasticity. In addition, the cosmetic composition for anti-aging or reverse aging according to the present disclosure exhibits an effect of preventing or alleviating skin aging by selectively removing senescent fibroblasts accumulated in the skin through the senescent cell death (senolytic) efficacy of ginsenoside.

Description

Cosmetic composition for skin improvement containing ginsenosides

[0001] The present application claims priority based on Korean application No. 10-2025-0010691 filed on January 23, 2025 and Korean application No. 10-2026-0013213 filed on January 22, 2026, and all contents disclosed in the specification and drawings of said application are incorporated by reference into the present application.

[0002] The present disclosure relates to a cosmetic composition for improving skin comprising ginsenosides.

[0003] The skin is the largest organ in the human body and performs various physiological roles, such as protecting the body from the external environment, maintaining moisture, regulating body temperature, and sensory functions. However, structural and functional changes in the skin occur with aging, which cause apparent aging, manifesting as wrinkle formation, loss of elasticity, dryness, and pigmentation.

[0004] One of the important mechanisms of skin aging is the aging-related changes in fibroblasts within the skin. Senescent fibroblasts undergo irreversible cessation of cell proliferation and acquire resistance to apoptosis, making them difficult to eliminate by the immune system. The senescence-associated secretory phenotype (SASP) refers to inflammatory cytokines, proteolytic enzymes, or growth factors secreted by senescent cells. These SASPs are known to induce aging in surrounding normal cells and exacerbate inflammatory conditions within the skin.

[0005] In addition, senescent fibroblasts inhibit the production of the extracellular matrix (ECM), leading to reduced collagen synthesis and consequently accelerating skin aging, which results in reduced skin volume, wrinkle formation, and decreased elasticity. Therefore, effectively inhibiting or removing these senescent fibroblasts is recognized as a key task in maintaining skin youth.

[0006] In this regard, senotherapeutic approaches have recently been attracting attention. These are classified into senolytic efficacy, which removes senescent cells from tissues by inducing their selective death, and senomorphic efficacy, which blocks the propagation of aging signals to surrounding tissues by inhibiting the expression of SASPs. In fact, there have been reports of cases where the application of certain senotherapeutic agents to the skin has induced histological improvement along with increased collagen synthesis, thereby alleviating apparent aging.

[0007] Meanwhile, hyaluronic acid also plays an important role in maintaining skin hydration and elasticity. Hyaluronic acid is abundant primarily in the extracellular matrix (ECM) within the dermis and possesses the ability to store approximately 1,000 times its own weight in water; therefore, it is essential for maintaining skin moisture balance, promoting tissue regeneration and wound healing, and preserving skin elasticity. However, as we age, the content of hyaluronic acid also decreases, leading to more pronounced signs of aging such as dryness, roughness, and loss of elasticity.

[0008] Therefore, there is an urgent need to develop high-performance cosmetic materials capable of treating aged fibroblasts and inducing the biosynthesis of collagen and hyaluronic acid, and this is emerging as a critical technological challenge for maintaining skin health and anti-aging skin care in an aging society.

[0009] Therefore, the problem that the present disclosure aims to solve is to provide a cosmetic composition with excellent effects in improving skin wrinkles and elasticity.

[0010] In addition, the problem that the present disclosure aims to solve is to provide a cosmetic composition having excellent skin anti-aging and reverse-aging effects.

[0011] As a result of researching various natural ingredients to improve skin aging phenomena, the inventors of the present disclosure discovered that among the various types of ginsenosides (Re, Rh1, CK, Rg1, or Rc, etc.), ginsenoside C-Mc1 surprisingly showed significantly superior effects in improving skin wrinkles, improving skin elasticity, anti-aging effects, and reverse aging effects.

[0012] The present disclosure provides a cosmetic composition for improving skin wrinkles or skin elasticity, comprising ginsenoside C-Mc1 as an active ingredient. In one aspect of the present disclosure, the "wrinkle improvement" effect may mean inhibiting or hindering the formation of wrinkles on the skin, or alleviating wrinkles that have already formed. Additionally, the "skin elasticity improvement" effect may mean that the structural and mechanical properties of the skin tissue are improved, thereby increasing the skin's resistance to deformation from external stimuli and its ability to recover to its original state after deformation. Furthermore, the present disclosure provides a cosmetic composition for anti-aging or reverse aging, comprising ginsenoside C-Mc1 as an active ingredient. The anti-aging or reverse aging cosmetic composition may be used for skin senescent cell apoptosis (senolytic) purposes, and through such senescent cell apoptosis efficacy, it may exhibit significant anti-aging or reverse aging effects on the skin.

[0013] In one aspect of the present disclosure, ginsenoside C-Mc1 can exert an senescent apoptotic effect by acting on aged fibroblasts accumulated in skin tissue to induce the death of such cells. Aged fibroblasts are difficult to naturally eliminate through the body's immune mechanisms (anti-apoptosis) and therefore persist in skin tissue; their accumulation acts as a factor that accelerates the progression of skin aging. Ginsenoside C-Mc1 can promote the selective elimination of aged fibroblasts by activating apoptosis-related signaling pathways. Accordingly, the restoration of normal fibroblast function is induced, and the synthesis of skin ECM components, including collagen and hyaluronic acid, is promoted, thereby improving the structural stability and elasticity of skin tissue.

[0014] As senescent cells are removed, the chronic inflammatory state within the skin is alleviated, and the activity of surrounding normal fibroblasts is restored, resulting in effects such as increased collagen synthesis and promotion of hyaluronic acid production. Consequently, wrinkles are improved, skin elasticity is increased, and this contributes to the overall regeneration of skin tissue and the maintenance of youth. The cosmetic composition of the present disclosure can be utilized as a functional composition that provides multiple anti-aging effects, such as visible improvement of apparent aging, restoration of skin metabolic function, and improvement of skin elasticity and moisture retention, based on the senescent cell apoptosis action that selectively kills senescent cells within the skin through ginsenoside C-Mc1.

[0015] In one aspect of the present disclosure, the active ingredient ginsenoside C-Mc1 may be included in the composition in an effective amount capable of sufficiently achieving efficacy in improving skin wrinkles or skin elasticity, or anti-aging or reverse-aging efficacy. The ginsenoside C-Mc1 may be included in an amount of 0.00005 to 10 weight%, preferably 0.0001 to 5 weight%, relative to the total weight of the composition. Alternatively, the ginsenoside C-Mc1 may be included in an amount of 0.00005 to 10 weight%, 0.00005 to 5 weight%, 0.00005 to 1 weight%, 0.0001 to 10 weight%, 0.0001 to 5 weight%, or 0.0001 to 1 weight% relative to the total weight of the composition. Within the above range, excellent efficacy in improving skin wrinkles and anti-aging is exhibited, and there is an advantage in that the formulation of the composition is stabilized.

[0016] In one aspect of the present disclosure, the cosmetic composition for improving skin wrinkles, improving skin elasticity, anti-aging, or reverse aging may further include one or more of quercetin, resveratrol, and kaempferol as additional active ingredients in addition to ginsenoside C-Mc1, and preferably may include all of quercetin, resveratrol, and kaempferol. Through the combination, the composition of the present disclosure may exhibit a significant synergistic effect for anti-aging.

[0017] In one aspect of the present disclosure, the cosmetic composition of the present disclosure for improving skin wrinkles, improving skin elasticity, anti-aging, or reverse aging may be prepared in various formulations that can be applied topically to the skin. The composition may be implemented in the form of a cream, lotion, essence, ampoule, gel, mask pack, mist, oil, balm, or stick, which are general external cosmetic forms.

[0018] In addition, the above composition may further include various conventional cosmetic additives for skin stability, improved usability, enhanced moisturizing power, and improved functionality, in addition to ginsenoside C-Mc1. Such additives may include skin-friendly oil phase components (e.g., jojoba oil, argan oil, etc.) and water phase components (e.g., purified water, glycerin, butylene glycol, etc.), surfactants for emulsion stabilization (e.g., polyglyceryl series, sorbitan fatty acid esters, etc.), and viscosity modifiers (e.g., carbomer, hydroxyethylcellulose, etc.).

[0019] In addition, additional ingredients for improving skin function may include moisturizers (e.g., hyaluronic acid, ceramide), antioxidants (e.g., vitamin E, coenzyme Q10), anti-inflammatory and soothing agents (e.g., madecassoside, centella extract), anti-wrinkle agents (e.g., adenosine, retinol), whitening agents (e.g., niacinamide), peptides, or skin regeneration-promoting ingredients (e.g., EGF). Furthermore, preservatives, fragrances, colorants, pH adjusters, or antioxidants may be added as needed to maintain stability.

[0020] In one aspect of the present disclosure, the cosmetic composition of the present disclosure may be classified as a functional cosmetic according to efficacy such as wrinkle improvement or elasticity improvement, and may also be applied as a quasi-drug.

[0021] Furthermore, the present disclosure provides a use for a composition comprising ginsenoside C-Mc1 as an active ingredient for improving skin wrinkles or skin elasticity. Specifically, the present disclosure includes a use of ginsenoside C-Mc1 as a key ingredient in the manufacture of a formulation (e.g., cosmetics, topical skin preparations, etc.) used for the purpose of improving signs of skin aging, particularly inhibiting the formation of wrinkles, alleviating existing wrinkles, or improving a decline in skin elasticity. In this case, the ginsenoside C-Mc1 may be incorporated in an amount capable of exhibiting an effective effect relative to the total weight of the final composition.

[0022] Furthermore, the present disclosure provides a method for improving skin wrinkles or skin elasticity, comprising the step of applying ginsenoside C-Mc1 or a composition containing it as an active ingredient to the skin of a subject who requires it. The subject refers to a mammal who requires prevention, improvement, or treatment of skin wrinkles or who desires to improve skin elasticity, and preferably includes a human. The application includes all conventional methods of skin application in which the composition of the present disclosure is applied directly to the surface of the subject's skin, sprayed, or absorbed. The method according to the present disclosure may include continuously applying a cosmetic composition containing an effective amount of ginsenoside C-Mc1 one to several times daily for a predetermined period (e.g., one week or more, four weeks or more, etc.). Through such an application method, skin wrinkles and elasticity can be significantly improved by promoting the synthesis of collagen and hyaluronic acid in the skin and by killing and controlling senescent cells.

[0023] All ingredients described in the present disclosure preferably do not exceed the maximum usage limits prescribed by relevant laws and regulations in countries such as Korea, China, the United States, Europe, and Japan (e.g., regulations on cosmetic safety standards, etc. (Korea), cosmetic safety technical standards (China), etc.). Preferably, the cosmetic or quasi-drug composition according to the present disclosure includes the ingredients according to the present disclosure within the content limits permitted by the relevant laws and regulations of each country.

[0024] The cosmetic composition for improving skin wrinkles or elasticity according to the present disclosure significantly increases the biosynthesis of collagen and hyaluronic acid within the skin, thereby exhibiting an effect of inhibiting wrinkle formation and improving it. Furthermore, the cosmetic composition for anti-aging or reverse aging according to the present disclosure exhibits an effect of preventing or improving skin aging by selectively removing senescent fibroblasts accumulated within the skin through the senolytic efficacy of ginsenosides.

[0025] Figure 1 shows the results of evaluating the senescent cell apoptosis efficacy of four types of ginsenosides in Experimental Example 4.

[0026] FIGS. 2a to 2d show the results of evaluating the senescent cell-regulating efficacy of lipid capsules containing quercetin, resveratrol, and kaempferol by measuring the expression levels of SASP-associated gene markers in Experimental Example 5 (CM-NF: culture medium obtained from normal cells, CM-SF: culture medium obtained from senescent cells).

[0027] Figure 3 is a graph showing the synergistic effect of the combination of ginsenoside, quercetin, resveratrol, and kaempferol on senescent cell death in Experimental Example 6.

[0028] Hereinafter, the present invention will be described in detail with reference to examples and the like to aid in understanding the invention. However, the embodiments according to the present invention may be modified in various different forms, and the scope of the present invention should not be interpreted as being limited to the following embodiments. The embodiments of the present invention are provided to more completely explain the invention to those with average knowledge in the field to which the invention pertains.

[0029]

[0030] Experimental Example 1: Skin cell culture

[0031] For evaluation, human skin-derived fibroblast cell line Hs68 (ATCC) and human keratinocyte cell line HaCaT (ATCC) were used. DMEM medium supplemented with 10% FBS and 1% penicillin-streptomycin was used in T175 flasks, and the cells were cultured at 37°C in a 5% CO2 incubator.

[0032]

[0033] Experimental Example 2: Evaluation of Collagen Synthesizing Ability of 4 Types of Ginsenosides

[0034] In this experimental example, to evaluate the effect of ginsenoside C-Mc1 on collagen synthesis in skin fibroblasts, Hs68 cells cultured in Experimental Example 1 were 5X10 4Cells were seeded into a 24-well plate at a cell-to-well ratio. After the cells had stably attached, they were treated with ginsenosides C-Mc1, Re, Rh1, or CK at concentrations of 1 ppm and 2 ppm, respectively, while the control group was not treated with ginsenosides.

[0035] After incubating for 24 hours following treatment with the substance, the supernatant was collected, and the secretion of collagen I alpha 1 (COL1A1) protein was analyzed using an enzyme-linked immunosorbent assay (ELISA) kit. The ELISA analysis was performed according to the manufacturer's protocol, and absorbance was measured at 450 nm. The collagen concentration was calculated by substituting the obtained data into a regression equation derived from the standard curve. The measured collagen content was converted into a relative value (%) based on the untreated group (100%) for comparative analysis. The results of the collagen synthesis ability evaluation for each ginsenoside are expressed as mean ± standard error and are shown in Table 1 below.

[0036] Treatment Concentration (ppm) Mean Standard Error C-Mc 12 16 6.8 0.6 11 5 9.7 0.5 Re 2 14 1.3 5.8 11 22.7 7.0 Rh 12 10 8.2 1.4 11 22.6 16.8 C-K 2 13 1.1 5.3 11 15.6 5.5

[0037] Experimental results confirmed that ginsenoside C-Mc1 induced significantly higher COL1A1 synthesis compared to other ginsenosides (Re, Rh1, CK) at concentrations of both 1 ppm and 2 ppm. This suggests that the C-Mc1 treatment group exhibits significantly superior efficacy in improving skin wrinkles, skin elasticity, anti-aging, and reverse aging compared to other ginsenosides.

[0038]

[0039] Experimental Example 3: Evaluation of Hyaluronic Acid Synthesis Ability of 4 Types of Ginsenosides

[0040] To evaluate hyaluronic acid synthesis ability, HaCaT cells cultured in Experimental Example 1 above were 5X10 4 Cells were seeded into a 24-well plate at a cell-to-well ratio. After the cells had stably attached, ginsenoside C-Mc1 was treated at concentrations of 1 ppm and 5 ppm, respectively, and an untreated group was set as a control. Additionally, ginsenosides Re, Rh1, and CK were treated at the same concentrations (1 ppm, 5 ppm) as comparative examples.

[0041] Incubation was carried out for 24 hours after sample treatment, and the cell culture supernatant was collected to measure the hyaluronic acid content using an ELISA kit. The ELISA analysis was performed according to the manufacturer's protocol, and absorbance was measured at 450 nm. The hyaluronic acid concentration was calculated by substituting the obtained data into a regression equation derived from the standard curve. The measured hyaluronic acid content was converted into a relative value (%) based on the untreated group (100%) for comparative analysis.

[0042] Treatment Concentration (ppm) Mean Standard Error C-Mc 157 42.4 159.0 195 4.7 40.6 Re 516 3.4 0.3 1319.0 29.0 Rh 1512 7.9 6.6 194.4 2.5 C-K 55 6.4 5.2 111 5.5 2.4

[0043] Looking at the experimental results shown in Table 2, ginsenoside C-Mc1 showed an increase in hyaluronic acid synthesis of approximately 955% in the 1 ppm treatment group and approximately 742% in the 5 ppm treatment group, demonstrating an effect that was improved by about 7 to 10 times compared to the untreated group. On the other hand, other ginsenosides at the same concentration showed relatively low increases in hyaluronic acid synthesis, confirming that the hyaluronic acid synthesis efficacy of C-Mc1 is particularly superior.

[0044]

[0045] Experimental Example 4: Evaluation of the Senolytic Efficacy of 4 Types of Ginsenosides

[0046] In this experimental example, the selective cell death effect (senolytic effect) induced by ginsenosides in normal cells and senescent cells was evaluated using Annexin V and PI (propidium iodide) staining.

[0047] Hs68 cells cultured in Experimental Example 1 above were 1X10 5 Cells were seeded into a 6-well plate at a cell-to-well ratio, and after the cells had stably attached, a specific dose of ultraviolet B (UVB) was irradiated to induce an aging model. Normal cells that had not been irradiated with UV were used as the control group.

[0048] Senescent cells and normal cells were treated with ginsenoside C-Mc1, Re, Rh1, or CK at concentrations of 1 ppm or 2 ppm, respectively, and cultured for 24 hours. After washing with PBS, the cells were collected. The collected cells were diluted in 1X binding buffer, followed by the addition of Annexin V-FITC and PI, and incubated in the dark for 15 minutes. The prepared samples were measured and analyzed using a flow cytometer.

[0049] When apoptosis occurs, phosphatidylserine (PS), a lipid forming the cell membrane, moves from the inner membrane to the outer membrane; therefore, the stage of cell death can be determined based on the detection level of PS. Since Annexin V binds to PS on the cell membrane and PI binds to the nucleus in terminally apoptotic and necrotic cells, simultaneous staining with Annexin V and PI allows for the identification of both early and terminally apoptotic cells. The ratio of cells positive for Annexin V and PI was defined as the "apoptosis induction rate," and the rate was converted into a relative value using the apoptosis induction rate of the untreated group as a baseline of 100%. The results of the senescent cell apoptosis efficacy evaluation were expressed as mean ± standard error and are shown in Table 3 and Figure 1 below.

[0050] Treatment Concentration (ppm) Aging Cells Normal Cells Mean Standard Error Mean Standard Error C-Mc 1 2 1 4 4.7 4.3 1 1 2.3 1 7.5 1 1 3 0.2 3.8 5 6.3 1 1.0 Re 2 1 1 7.8 0.2 8 6.1 1.3 1 7 6.6 7.8 8 5.8 1 0.2 Rh 1 2 1 2 0.0 1 1.1 1 1 4.1 1 3.0 1 9 5.8 9.7 1 0 5.8 2.8 C-K 2 1 1 7.1 1.5 8 7.7 8.2 1 6 9.0 4.9 6 7.2 7.5

[0051] It was found that the greater the ability to induce apoptosis in senescent cells without inducing death in normal cells, the greater the effect on senescent cell apoptosis. In the groups treated with 1 ppm and 2 ppm of ginsenoside C-Mc1, the apoptosis induction rate for normal cells was similar to or lower than that of the control group, while the apoptosis induction rate for senescent cells was significantly higher, averaging 130.2% and 144.7%, respectively. In contrast, the apoptosis induction rates for senescent cells in the groups treated with ginsenosides Re, Rh1, and CK did not reach this level. In other words, it was confirmed that ginsenoside C-Mc1 has a significantly higher efficacy in selectively killing senescent cells compared to other ginsenosides.

[0052]

[0053] Experimental Example 5: Evaluation of Senomorphic Efficacy of a Composition Containing Quercetin, Resveratrol, and Kaempferol

[0054] Lipid capsules containing quercetin, resveratrol, and kaempferol as active ingredients were prepared according to a conventional method with the composition listed in Table 4 below.

[0055] Composition Lipid Phase 1: Glyceryl Behenate 3.6, Glyceryl Stearate 0.6, Glyceryl Distearate 0.6, Cetyl Palmitate 0.6, Myristyl Myristate 0.6, Hydrogenated Lecithin 0.2 Lipid Phase 2: Caprylic / Capric Triglyceride 2.4, Polysorbate 20 3.5, Quercetin 0.1, Resveratrol 0.1, Kaempferol 0.01 Aqueous Phase: Polysorbate 60 0.7, Poloxamer 18 8 0.7, Sodium Stearoyl Glutamate 0.6, Distilled Water up to 100

[0056] Normal fibroblasts (HS68) or fibroblasts induced by UV aging were cultured in well plates, and the culture medium was collected from each. At the same time, the culture medium of aging fibroblasts cultured with the lipid capsules at concentrations of 0.1% or 0.01% was also collected. Subsequently, each culture medium was applied to normal cells to observe the difference in the degree of aging spread. To this end, the expression levels of SASP-associated gene markers were measured, and the results are shown in Figures 2a to 2d. When normal cells were treated with the simple culture medium of aging cells, the expression levels of SASP-associated genes increased, indicating that aging was accelerated by the culture medium of aging cells. On the other hand, when normal cells were treated with the culture medium of aging cells cultured with the lipid capsules, cellular aging was not intensified, and the level approached that of normal cell culture medium, exhibiting a seneomorphic effect.

[0057]

[0058] Experimental Example 6: Synergistic effect of a combination of ginsenoside, quercetin, resveratrol, and kaempferol on apoptosis

[0059] In this experimental example, the senescent cell apoptosis effects of ginsenoside alone or a combination of ginsenoside and quercetin, resveratrol, and kaempferol (QRK) were compared. Wild ginseng ginsenoside (WGG) was used as the ginsenoside alone, which is a complex ginsenoside composition containing ginsenoside C-Mc1. The senescent cell apoptosis effect observed in this complex composition can be interpreted as being expressed by the action of the individual ginsenosides included in the composition. In particular, ginsenoside C-Mc1 is a component closely associated with the senescent cell regulation mechanism proposed in the present invention, and the results of this experiment suggest that a similar effect can be expected even when ginsenoside C-Mc1 is used as an active ingredient.

[0060] It can be seen that the greater the ability to selectively kill senescent cells without inducing the death of normal cells, the greater the effect of senescent cell death. Specifically, UVB 20 mJ / cm² on fibroblasts 2 Cellular senescence was induced by irradiation, and aged fibroblasts were cultured in well plates. The cultures were treated with either a ginsenoside-only experimental group or a ginsenoside and QRK mixture in a 1:1 ratio. Subsequently, Annexin V and PI staining were performed in the same manner as in Experimental Example 4 to compare the cell death induction rate (%). Figure 3 shows the proportion of cells that tested positive for Annexin V and PI. Based on the experimental results shown in Figure 3, it was confirmed that the ginsenoside and QRK mixture in a 1:1 ratio exhibited a significant synergistic effect on senescent cell death compared to the ginsenoside-only treatment group.

Claims

1. A cosmetic composition for improving skin wrinkles or skin elasticity, comprising ginsenoside C-Mc1 as an active ingredient.

2. A cosmetic composition for anti-aging or reverse aging containing ginsenoside C-Mc1 as an active ingredient.

3. In paragraph 2, the cosmetic composition is a cosmetic composition that exhibits an anti-aging or reverse-aging effect through the efficacy of inducing apoptosis in skin aging cells.

4. A cosmetic composition for skin aging cell apoptosis containing ginsenoside C-Mc1 as an active ingredient.

5. A cosmetic composition according to any one of claims 1 to 4, wherein the composition comprises 0.00005 to 10 weight% of ginsenoside C-Mc1 based on the total weight of the composition.

6. A cosmetic composition according to any one of claims 1 to 4, wherein the composition additionally comprises one or more of quercetin, resveratrol, and kaempferol.

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