KR102128260B1 - Cosmetics composition containing amide compound - Google Patents

Abstract

The present invention relates to a cosmetic composition for skin protection against active oxygen species, ultraviolet rays, or blue light comprising an amide compound. The cosmetic composition according to the present invention inhibits or eliminates production of the active oxygen species, increases expression of SIRT1 reduced by the active oxygen species, and suppresses expression levels of various genes related to cell growth. Therefore, a skin condition is improved as well as the skin protection. The cosmetic composition for the skin protection against the active oxygen species, the ultraviolet rays, or the blue light includes N-(2-hydroxyethyl)-2-butyl-octanamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexanamide, N-(2-hydroxyethyl)-2,4,5-trimethyl-benzamide, or combinations of the same.

Description

Cosmetic composition containing amide compound {COSMETICS COMPOSITION CONTAINING AMIDE COMPOUND}

The present invention relates to a cosmetic composition comprising an amide-based compound, specifically, to an active oxygen species containing an amide-based compound, a cosmetic composition for skin protection against ultraviolet light or blue light.

Ultraviolet rays are the wavelengths irradiated from sunlight and are the main cause of erythema, edema, freckles, and skin cancer on the skin. In general, ultraviolet rays are classified into ultraviolet rays A (320-400 nm), ultraviolet rays B (280-320 nm) and ultraviolet rays C (240-280 nm) according to their wavelengths. The ultraviolet A is characterized by long wavelength and low energy, and is known to induce skin damage and skin irritation by infiltrating the dermis of the skin, promoting skin cancer, wrinkles, and melanin formation, but the intensity of energy is not high. Ultraviolet B is characterized by short wavelength and high energy, and among the ultraviolet rays, it is the most biologically influential to the human body and is the main cause of light damage to the skin. Since the ultraviolet B has a high energy intensity, it penetrates to the epidermis of the skin and causes erythema, freckles, and edema. In addition, chronic exposure to the ultraviolet B results in skin damage, immune suppression, skin cancer and apoptosis. UV C passes through the ozone layer and does not reach the surface and disappears.

In recent years, in order to suppress skin damage caused by ultraviolet rays, the use of sunscreens that protect cells by blocking the penetration of ultraviolet rays or components that have the function of inhibiting the production of free radicals in the cells by ultraviolet rays Development is actively taking place.

An object of the present invention is to provide a cosmetic composition for protecting skin against reactive oxygen species, ultraviolet rays or blue light.

An object of the present invention is to provide a cosmetic composition capable of protecting skin by effectively suppressing or removing skin without irritation of free radicals caused by ultraviolet light or blue light.

An object of the present invention is to provide a cosmetic composition capable of protecting skin by increasing SIRT1' expression and preventing the death of skin cells.

An object of the present invention is to provide a cosmetic composition capable of protecting skin by inhibiting the expression of phosphorylated Hihstone H2A.X (Phospho-Histone H2A.X) and p16.

An object of the present invention is to provide a cosmetic composition capable of inhibiting SA beta-galactosidase expression and protecting the skin.

For the above-mentioned purposes, in the present invention, N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide , N-(2-hydroxyethyl)-2,4,5-trimethyl-benzamide or a combination thereof, as an active ingredient, an active oxygen species, and a cosmetic composition for protecting skin against ultraviolet light or blue light.

The cosmetic composition according to an embodiment of the present invention may exhibit skin protection activity by inhibiting or removing the generation of reactive oxygen species generated due to ultraviolet rays or blue light.

The cosmetic composition according to an embodiment of the present invention may be to increase the expression of SIRT1.

The cosmetic composition according to an embodiment of the present invention may be to suppress the expression of phosphorylated Hihstone H2A.X (Phospho-Histone H2A.X) and p16.

The cosmetic composition according to an embodiment of the present invention may be to suppress SA beta-galactosidase expression.

In the cosmetic composition according to an embodiment of the present invention, the active ingredient may be included as 0.001 to 5% by weight relative to the total weight.

The cosmetic composition according to an embodiment of the present invention may be formulated with softening makeup, converging makeup, nutritional makeup, eye cream, nutritional cream, massage cream, cleansing cream, cleansing foam, cleansing water, essence or pack, etc. .

In the present invention, a novel compound represented by the following structure, namely, N-(2-hydroxyethyl)-2-butyl-octanamide is provided.

In the present invention, N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide, N-( A method of improving skin condition using a composition comprising 2-hydroxyethyl)-2,4,5-trimethyl-benzamide or a combination thereof as an active ingredient is provided.

In a method according to an embodiment of the present invention, the improvement comprises inhibiting and eliminating the production of reactive oxygen species; Increased expression of SIRT1; Inhibition of the expression of phosphorylated Hihstone H2A.X and p16; And SA beta-galactosidase expression.

According to the present invention, it is possible to effectively suppress or eliminate the generation of reactive oxygen species caused by internal and external changes in the skin, and increase the reduced SIRT1　 expression by the reactive oxygen species, thereby protecting the skin. In addition, by suppressing skin cell damage caused by free radicals, ultraviolet rays or blue light, it exhibits excellent efficacy in protecting skin cell damage.

According to the present invention, by suppressing the expression level of genes related to cell growth, it can be effective in skin protection as well as improvement of skin condition. In addition, it is safe for the human body and does not cause side effects even for long-term use, thereby providing the advantage of being capable of exerting a significant effect as a composition for protecting and improving skin damage by free radicals, ultraviolet light, or blue light.

1 is a view showing the activity change of reactive oxygen species after UV irradiation,
2 is a view showing the expression level of the SIRT1 gene after UV irradiation,
Figure 3 is a diagram showing the level of expression of the histones H2A.X and p16 ^INK4A phosphorylation after irradiation with ultraviolet light,
4 is a view showing the effect on SA beta-galactosidase activity after UV irradiation.

The cosmetic composition comprising the amide-based compound according to the present invention will be described below, but unless otherwise defined in the technical terms and scientific terms used at this time, those skilled in the art to which the present invention pertains generally understand and In the following description, descriptions of well-known functions and configurations that may unnecessarily obscure the subject matter of the present invention are omitted.

The term "Reactive oxygen species (ROS)" in this specification is oxygen in an unstable state, and is an overproduction of oxygen due to environmental pollution, chemicals, ultraviolet rays, blood circulation disorders, and stress. Reactive oxygen species cause oxidative action in the human body, for example, damage to cell membranes, DNA, and all other cell structures, and their function may be lost or altered depending on the extent of the damage. In addition, free radicals in skin cells cause oxidative stress.

As used herein, the term "ultraviolet rays" is classified into ultraviolet A (320-400 nm), ultraviolet B (280-320 nm), and ultraviolet C (240-280 nm) according to its wavelength. Ultraviolet rays refer to light sources that directly damage skin cells and indirectly damage them through the generation of reactive oxygen species. The generation of reactive oxygen species is regulated by the antioxidant defense system, but when excessively reactive oxygen species are generated due to pollution, solar ultraviolet rays, chemical oxidizing agents, and microorganisms, these defense systems are destroyed, and as a result, the cells are oxidized to DNA, lipids, and proteins. Oxidative stress caused by damage and ultraviolet rays may cause skin inflammation and cell death.

As used herein, the term “blue light” means a light source having a wavelength between 380 and 500 nm. In particular, blue light, which is known to come from electronic devices such as LED lamps, smartphones, and computers, has higher energy than visible light of other wavelengths and is frequently exposed in everyday life, causing adverse effects on skin.

The present inventors continued to study cosmetic materials, while the amide-based compound of a specific structure exerts an excellent effect on the scavenging effect of free radicals derived from ultraviolet or blue light as well as free radicals induced by hydrogen peroxide. It was confirmed that it exerts an excellent effect on increasing the expression of SIRT1. However, it was found that compounds with similar structural characteristics also showed non-specific effects, which furthered the study.

The present inventors, in particular, N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide, N-( 2-hydroxyethyl)-2,4,5-trimethyl-benzamide. The amide-based compound described above is excellent in the effect of increasing the expression amount of SIRT3 reduced by the reactive oxygen species as well as the remarkable scavenging effect of the reactive oxygen species. In addition, it was confirmed that the effective amount of the amide-based compound showing the scavenging effect of free radicals was not cytotoxic in experiments using a human dermal fibroblast. Accordingly, the present inventors intend to propose the present invention based on such effects, by revealing their previously unknown uses and surprisingly significantly improved effects in these uses.

Hereinafter, the present invention will be described in detail.

The cosmetic composition of the present invention is N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide, N- (2-Hydroxyethyl)-2,4,5-trimethyl-benzamide or a combination thereof as an active ingredient, the specific function of which is as follows.

The cosmetic composition of the present invention may be a cosmetic composition for skin protection against reactive oxygen species, ultraviolet light or blue light. In addition, the active oxygen species is not limited as long as it is an over-produced oxygen species that causes oxidative stress on the skin, but for example, it may be selected from hydrogen peroxide, superoxide anion, and hydroxy radical.

Specifically, the cosmetic composition of the present invention, ⅰ) the scavenging effect of reactive oxygen species derived from ultraviolet light or blue light, ii) the effect of increasing the expression of SIRT1, and iii) the effect of inhibiting the expression of phosphorylated 　histone H2A.X and p16. Iv) By implementing the SA beta-galactosidase expression inhibitory effect, it is possible to protect the skin and at the same time improve the collapse of skin homeostasis.

In addition, the cosmetic composition of the present invention protects cells from apoptosis by inhibiting apoptosis as well as reactive oxygen species derived from ultraviolet light or blue light.

The cosmetic composition of the present invention can be simultaneously implemented for the above effects. That is, the cosmetic composition of the present invention exhibits an effective effect in improving skin cell damage caused by these as well as skin protection effects against reactive oxygen species, ultraviolet rays or blue light, and can be effectively used in skin protection applications.

In addition, the present invention can also be used as a method of improving the condition of the skin by applying the cosmetic composition of the present invention described above to the skin. The improvement is changed to a more beneficial skin condition by a combination of the above-described effects, and the effect of the present invention must be an excellent effect realized at the cellular level.

In addition, it is expected that various skin information may be screened based on such effects, and usefully used for providing beauty information about the skin.

The cosmetic composition of the present invention is N-(2-hydroxyethyl)-2-butyl-octanamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexane as described above. Characterized in that it comprises an amide-based compound selected from amide, N-(2-hydroxyethyl)-2,4,5-trimethyl-benzamide and combinations thereof, as an active ingredient, and the amide-based compound has the following structure Have

As an example, the cosmetic composition of the present invention as an active ingredient, the pharmaceutically acceptable salt of the amide-based compound, solvate thereof and stereoisomers thereof may also be included as an aspect of the present invention.

The cosmetic composition of the present invention effectively inhibits or eliminates the production of free radical species and thus exhibits skin protection activity.

The cosmetic composition of the present invention increases SIRT1' expression and prevents the death of skin cells, thereby protecting the skin and improving the skin condition. In addition, it is possible to effectively inhibit the cell membrane oxidation as well as damage the DNA of the cell.

In addition, the cosmetic composition of the present invention protects the skin by inhibiting the expression of phosphorylated Phospho-Histone H2A.X and p16 and inhibiting SA beta-galactosidase expression. The phosphorylated Hihstone H2A.X (Phospho-Histone H2A.X), p16 and SA beta-galactosidase, etc., are genes related to cell growth, and when their expression levels are suppressed, they may be effective in improving the skin condition. The cosmetic composition of the invention relates to suppression of expression of these genes. Thus, the cosmetic composition of the present invention can simultaneously induce the suppression of expression of these genes, thereby providing excellent synergy in improving the skin condition.

In addition, the amide-based compound can be safely used as it does not cause cytotoxicity and skin irritation at a dose that expresses effective effects on the skin. In addition, the amide-based compound not only does not cause a phenomenon of sedimentation or separation in the formulation, as well as maintaining its efficacy stably in the formulation, as well as good storage stability.

In the cosmetic composition according to an embodiment of the present invention, the active ingredient may be included in 0.001 to 5% by weight based on the total weight of the cosmetic composition. Specifically, it is preferably contained in 0.001 to 3% by weight, more specifically 0.01 to 1% by weight. When the active ingredient is included in the above-described range, it is more preferable to show the desired effect in the present invention, that is, it is remarkable for use without impairing the stability of the formulation.

In addition, in the cosmetic composition according to an embodiment of the present invention, it may be possible to impart more significant synergies when the active ingredient is included in the form of a mixture. In particular, the N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide and N-(2- When a combination of two or more selected from hydroxyethyl)-2,4,5-trimethyl-benzamide is included as an active ingredient, it shows more remarkable effect on the scavenging effect of free radical species. Further, in the above effect, a combination containing N-(2-hydroxyethyl)-2-butyl-octaneamide is more preferable.

For example, in the case of the mixed active ingredient, the N-(2-hydroxyethyl)-2-butyl-octaneamide and N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2- Methyl-hexaneamide or N-(2-hydroxyethyl)-2,4,5-trimethyl-benzamide may be mixed in a weight ratio of 0.01:99.99 to 99.99:0.01, specifically 1:9 to 9:1 The weight ratio, more specifically, may be mixed in a weight ratio of 1:1 to 9:1, but is not limited thereto.

Cosmetic composition according to an embodiment of the present invention may be to include the above-described active ingredient and the residual amount of water, it can be of course formulated in various embodiments.

The cosmetic composition according to an embodiment of the present invention may be formulated into a general emulsifying formulation, a solubilizing formulation, or the like, using a commonly known manufacturing method.

For example, the cosmetic composition may be formulated in a formulation selected from softening makeup, converging makeup, nutritional makeup, eye cream, nutrition cream, massage cream, cleansing cream, cleansing foam, cleansing water, essence, pack, etc. It is not limited.

In addition, the cosmetic composition may further include additional additives as appropriate, as desired, and components selected from wrinkle-improving ingredients, antioxidant ingredients, and whitening ingredients known in the art together with the amide-based compounds. It can contain. For example, it may be selected from retinoic acid, TGF, protein derived from animal placenta, betulinic acid, and chlorella extract, but is not limited thereto.

In addition, the cosmetic composition is a stabilizer, emulsifier, thickener, moisturizer, liquid crystal film strengthening agent, pH adjusting agent, antibacterial agent, water-soluble polymer, coating agent, metal ion blocker, amino acid, organic amine, polymer emulsion, pH adjusting agent, skin nutritional agent, oxidation One or more aqueous additives selected from antioxidants, antioxidants, preservatives, fragrances, and the like; And one or more oil additives selected from oils and fats, waxes, hydrocarbon oils, higher fatty acid oils, higher alcohols, synthetic ester oils, and silicone oils.

In this case, each of the additives may be included in 0.001 to 20% by weight relative to the total weight of the cosmetic composition, specifically, 0.01 to 10% by weight, 0.05 to 5% by weight, but is not limited thereto.

(Assessment Methods)

1. Confirmation of the elimination effect of reactive oxygen species (ROS)

The effect of scavenging reactive oxygen species in Examples and Comparative Examples of the present invention was confirmed.

Image analysis of the occurrence of reactive oxygen species (ROS) in cells is performed by seeding 1Х10 ⁵ (100 μL/well) HDF (human dermal fibroblast) in a 12 well plate with a cover slip attached. Was performed. After exposure to long-wavelength ultraviolet (UVA) 500 mJ/cm ² , samples of Examples and Comparative Examples were treated with 100 μM and cells were additionally incubated at 37° C. for 24 hours. DCF-DA 100μM was added to each well and incubated at 37°C for 45 minutes. After washing with PBS, stained cells were placed on a microscope slide in a mounting medium. Micrographs were observed with fluorescent microscopic images.

The results obtained therefrom are shown in Fig. 1 below. The control (control) of Figure 1 is a test group that does not process the sample, (-) is the result of the state exposed to UVA in the experimental group.

2. Check the expression level of SIRT1

In order to measure the expression level of the SIRT1' gene of Examples and Comparative Examples of the present invention, a q-PCR method was used.

Specifically, the acquisition of mRNA from human dermal fibroblast (HDF) was performed by isolating RNA according to the manufacturer's instructions using easy BLUE reagent. Specifically, 2×10 ⁵ cells/dish cells were prepared in a 6-well plate, and cultured for 24 hours at 37° C. and 5% CO ₂ conditions. After exposure to long-wavelength ultraviolet (UVA) 500 mJ/cm ² , samples of Examples and Comparative Examples were treated with 100 μM. Thereafter, after removing the culture solution cultured for 24 hours, 1 mL of easy BLUE was added to obtain cells. Each of the obtained cells was transferred to a 1.5 mL microfuge tube, and 0.2 mL of chloroform was added to stand for 5 minutes at room temperature, followed by centrifugation at 15,000 rpm for 15 minutes. After performing the centrifugation, the supernatant of the mixed solution that destroyed the cells was transferred to a new 1.5 mL microfuge tube, and then inverted by adding 0.4 mL of isopropyl alcohol, left at room temperature (25°C) for 15 minutes, and 15 at 13,000 rpm. Obtained by centrifugation for a minute to precipitate RNA. After removing isopropyl alcohol from the tube, inverting by adding 1 mL of 75% ethanol, centrifuging at 10,000 rpm for 5 minutes to remove ethanol to obtain purified RNA, and when the RNA is completely dried, DEPC- RNA was obtained by adding DW.

The effect on SIRT1_mRNA concentration was confirmed by performing reverse trascription PCR. The relative concentration of mRNA obtained by performing reverse transcription PCR was obtained by comparing the mRNA concentration of β-actin gene, which is a housekeeping gene.

It measured the change in the amount of mRNA by Q-PCR using each specific primer.

The results obtained therefrom are shown in Fig. 2 below.

3. determine the expression level of p16 ^INK4A and phosphorylated Histone H2A.X (Phospho-Histone H2A.X)

It was confirmed that the expression level of the Examples and Comparative Examples Western blot (Western blot) and p16 ^INK4A phosphorylated histone with H2A.X (Phospho-Histone H2A.X) of the present invention.

Specifically, human dermal fibroblast (HDF) is 1×10 ⁵ (1 mL/well) in a 12 well plate containing Dulbecco's modified eagle medium (DMEM) medium containing 10% fetal bovine serum (FBS). The dog was attached. After incubation for 24 hours, it was replaced with 1% fetal calf serum. After exposure to long-wavelength ultraviolet (UVA) 500 mJ/cm ² , samples of Examples and Comparative Examples were treated with 100 μM and cells were additionally incubated at 37° C. for 24 hours. That after the number of times the cells were analyzed for expression of Western blotting (western blot) the p16 ^INK4A in fibroblasts and phosphorylated Histone H2A.X (Phospho-Histone H2A.X) through with respect to each of these samples. The sample was used in Example 1 and Comparative Example 1 containing an amide-based compound of the structure shown in Table 1.

The results obtained therefrom are shown in Fig. 3 below.

4. Confirmation of the expression level of SA beta-galactosidase

In order to confirm the effect on SA beta-galactosidase　 activity of Examples and Comparative Examples of the present invention, a senescence assay was performed.

Specifically, a damaged human dermal fibroblast (HDF) was used. After seeding 1Х10 ⁵ (1 mL/well) of fibroblasts in 12 well plates, incubated for 24 hours, and treated with long-wave ultraviolet (UVA) 500mJ/cm ² . Samples of Examples and Comparative Examples were treated with 100 μM and cells were additionally incubated at 37° C. for 24 hours. Wash once with phosphate-buffered saline (PBS), fix the cells with 1X Fixative Solution for 15 minutes at room temperature, and remove the fixative. After adding 500 μl of the β-Galactosidase Staining Solution staining solution to a 12 well plate, wrapped in silver foil and reacted at 37° C. for 24 hours and observed with a microscopic image. The cells damaged by the SA-β-gal staining method stained the cytoplasm in blue, so an image was taken to confirm the number of stained cells compared to the total cells.

The results obtained therefrom are shown in Fig. 4 below.

(Examples 1 to 3)

The above evaluation method was carried out using an amide compound having the structure shown in Table 1 below. Samples to be used as the experimental group of each example were prepared in various concentrations according to each evaluation method.

The above Example 1 was a novel amide-based compound, and was prepared through the following synthetic method.

The reaction solution was prepared by adding dichloromethane (DCM, 375 mL, Samjeon Pure) and triethylamine (TEA, 26.1 mL, Samjeon Pure) to monoethanolamine (8.3 mL, 137.3 mmol, Sigma-Aldrich). After 10 minutes at room temperature, EDC.HCl (28.7 g, 149.8 mmol, Sigma-Aldrich)), HOBt (20.2 g, 149.8 mmol, Sigma-Aldrich), 2-butyloctanoic acid (2-butyloctanoic acid, 25.0 g, 124.8 mmol, Sigma-Aldrich) was added, followed by stirring at room temperature for 12 hours. Water was added to the reaction solution, stirred and allowed to stand, followed by layer separation. Water was added to the organic layer of the reaction solution, acidified with concentrated hydrochloric acid, stirred, allowed to stand, and then separated. The combined organic layers were washed with saturated salt (Brine), dried over sodium sulfate (Na ₂ SO ₄ ), filtered and the filtrate was concentrated under reduced pressure. The residue was purified by column chromatography to obtain a white solid compound (23.1 g, yield: 76%). The obtained solid was analyzed by MS (Agilent, USA) and NMR (Varian, USA). The analysis results are as follows.

¹ H-NMR (400 MHz, DMSO): 7.76 (brs, 1H), 4.60 (brs, 1H), 3.40-3.33 (m, 2H), 3.11-3.02 (m, 2H), 2.22-2.02 (m, 1H) ), 1.49-1.40 (m, 2H), 1.39-1.13 (m, 14H), 0.89-0.86 (m, 6H).

MS (ESI neg, ion) m/z: 242 (MH-). Calc'd exact mass for C ₁₄ H ₂₉ NO ₂ : 243.39

(Comparative Example 1)

The above evaluation method was carried out using an amide compound having the structure shown in Table 1 below. Samples of each comparative example were also prepared in various concentrations according to each evaluation method.

In all cases of the sample treated with the compound of the present invention, the production of reactive oxygen species was significantly reduced, and the removal of the produced reactive oxygen species was excellent. On the other hand, Comparative Example 1 did not exert a significant effect on the suppression of the generation of reactive oxygen species as well as the removal of the generated reactive oxygen species.

As shown in Figure 1 below, the sample treated with the compound of the present invention was excellent in the scavenging effect of reactive oxygen species generated from long-wave ultraviolet (UVA). Specifically, in the sample treated with the compound of the present invention (Example 1), the sample treated with Comparative Example 1 showed a remarkable scavenging effect of 450% compared to the experimental group exposed only to UVA, which increased to 1500%. It showed only 1200% erasing efficiency.

As shown in Figure 2, the sample treated with the compound of Example 1 of the present invention was confirmed that the SIRT1　mRNA expression increased more than 2 times compared to the experimental group exposed only UVA. On the other hand, in the sample treated with Comparative Example 1, no significant increase in SIRT1　mRNA expression was observed. Thus, it was confirmed that the compound of the present invention has an excellent effect of increasing the activity of reduced 　SIRT1 in skin cells by ultraviolet irradiation.

To the level of expression was found in 3, the UV post-treatment, Western blot analysis (western blot analysis) the histones H2A.X (Phospho-Histone H2A.X) phosphorylation and p16 ^INK4A by. The long-wavelength ultraviolet light (UVA) in a group 500 mJ / cm ² treatment was confirmed that the increase in the expression of the p16 ^INK4A and phosphorylated Histone H2A.X (Phospho-Histone H2A.X), which in humans by long wavelength ultraviolet light (UVA) It was suggested that it is sufficient to induce cell damage in fibroblasts. In addition, expression of the long-wavelength ultraviolet light (UVA) a histone H2A.X (Phospho-Histone H2A.X) phosphorylation and p16 ^INK4A which is increased by irradiation in order to determine whether the control by the compound of the present invention (Example 1) was observed that the expression of the decrease of the histones H2A.X (Phospho-histone H2A.X) phosphorylation and p16 ^INK4A by a long-wavelength ultraviolet light (UVA) at the conditions at a sample (example 1) after the irradiation treatment.

As shown in Figure 4, the sample treated with the compound of the present invention was confirmed that the amount of expression of SA beta-galactosidase was significantly reduced, and a change in cell morphology appeared.

As described above, the present invention has been described by specific matters and limited embodiments, but it is provided to help a more comprehensive understanding of the present invention, and the present invention is not limited to the above embodiments, and the field to which the present invention pertains Those skilled in the art can make various modifications and variations from these descriptions.

Accordingly, the spirit of the present invention should not be limited to the described embodiments, and should not be determined, and all claims that are equivalent or equivalent to the scope of the claims as well as the claims described below belong to the scope of the spirit of the invention. .

Claims (12)

N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide, N-(2-hydroxyethyl )-2,4,5-trimethyl-benzamide or a combination of these as an active ingredient, an active oxygen species, a cosmetic composition for skin protection against ultraviolet light or blue light. According to claim 1,
The cosmetic composition,
A cosmetic composition that inhibits or eliminates the production of free radical species. According to claim 2,
The reactive oxygen species,
Cosmetic composition, which is selected from hydrogen peroxide, superoxide anion and hydroxy radical. According to claim 3,
The cosmetic composition,
Cosmetic composition that inhibits or eliminates the production of free radicals caused by ultraviolet rays or blue light, thereby exhibiting skin protective activity. According to claim 1,
The cosmetic composition,
Cosmetic composition that increases the expression of SIRT1 (Silent Information Regulator 2-related protein type1). According to claim 1,
The cosmetic composition,
A cosmetic composition that inhibits the expression of phosphorylated histone H2A.X (Phospho-Histone H2A.X) and p16. According to claim 1,
The cosmetic composition,
SA beta-galactosidase (senescence-associated β-galactosidase) inhibits the expression and promotes cell migration, cosmetic composition. According to claim 1,
The active ingredient,
It is contained in 0.001 to 5% by weight relative to the total weight, cosmetic composition. According to claim 1,
The cosmetic composition,
Cosmetic composition that is formulated with softening lotion, converging makeup, nutritional makeup, eye cream, nutrition cream, massage cream, cleansing cream, cleansing foam, cleansing water, essence or pack. Compound represented by the following structure.

N-(2-hydroxyethyl)-2-butyl-octaneamide, N-(2-hydroxy-1-(hydroxymethyl)ethyl)-2-methyl-hexaneamide, N-(2-hydroxyethyl )-2,4,5-trimethyl-benzamide or a combination thereof as an active ingredient, using a composition as a cosmetic, a method of improving the skin condition. The method of claim 11,
The improvement,
Inhibit and eliminate the production of reactive oxygen species;
Increased expression of SIRT1;
Inhibiting the expression of phosphorylated histone H2A.X and p16; And
Method by inhibiting SA beta-galactosidase expression and promoting cell migration.

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