KR102106756B1 - Composition for preventing or treating skin damages caused by ultraviolet rays - Google Patents

Abstract

Disclosed herein is a composition for preventing or treating skin damage caused by ultraviolet rays comprising a peptide or a fragment thereof as an active ingredient. In particular, the composition containing the peptide according to the present invention has an advantage of excellent treatment or prevention effect on skin damage caused by both UVA and UVB.

Description

Composition for preventing or treating skin damages caused by ultraviolet rays}

The present specification relates to a composition for preventing or treating skin damage caused by ultraviolet rays containing a peptide derived from human protein as an active ingredient.

Telomere is a genetic material that is repeatedly present at the ends of chromosomes and is known to prevent damage to the chromosome or binding to other chromosomes. Each time a cell divides, the length of the telomeres decreases slightly, but if there is a cell division over a certain number of times, the telomeres become very short, and the cells stop dividing and die. On the other hand, it is known that prolonging telomeres prolongs the lifespan of cells, and for example, cancer cells secrete an enzyme called telomerase to prevent telomeres from shortening, so that cancer cells can continue to proliferate without dying.

European Patent Publication No. 1362597 European Patent Publication No. 0841396

One aspect of the present invention is to provide a peptide useful for the skin.

One aspect of the present invention is to provide a composition comprising a peptide derived from human protein as an active ingredient.

One aspect of the present invention is to provide a peptide having the efficacy of preventing or treating skin damage.

One aspect of the present invention is to provide a peptide useful for the prevention or treatment of skin damage caused by ultraviolet rays.

One aspect of the present invention is to provide a composition having the effect of preventing or treating skin damage caused by ultraviolet rays.

One aspect of the present invention is to provide a cosmetic composition having the effect of preventing or treating skin damage caused by ultraviolet rays.

One aspect of the present invention is to provide a health food composition having the efficacy of preventing or treating skin damage caused by ultraviolet rays.

One aspect of the present invention is to provide a pharmaceutical composition having the efficacy of preventing or treating skin damage caused by ultraviolet rays.

One aspect of the present invention comprises a peptide comprising SEQ ID NO: 1, a peptide having a sequence homology of 80% or more with the peptide sequence, or a fragment thereof as an active ingredient, in ultraviolet light having a function of alleviating cytotoxicity by ultraviolet light It provides a composition for preventing or treating skin damage caused by.

Another aspect of the present invention provides a composition having an excellent effect on preventing or treating skin damage caused by both UVA and UVB.

Another aspect of the present invention provides a cosmetic, pharmaceutical or health food composition comprising a composition for preventing or treating skin damage caused by ultraviolet rays.

The composition according to the present invention shows an effect of alleviating cytotoxicity caused by excellent ultraviolet rays by including a peptide comprising SEQ ID NO: 1, a peptide having 80% or more sequence homology with the peptide sequence, or a fragment thereof as an active ingredient. Therefore, it is possible to prevent or treat skin damage caused by ultraviolet rays by alleviating cytotoxicity caused by ultraviolet rays of the skin. In particular, the composition containing the peptide according to the present invention has an advantage of excellent treatment or prevention effect on skin damage caused by both UVA and UVB.

1 is a graph showing the results of measuring the cell viability (Cell viability,%) according to the cytotoxic alleviation effect by ultraviolet irradiation for the concentration change of the peptide of SEQ ID NO: 1 according to an aspect of the present invention.
2 is a graph showing the results of inhibiting IL-1α, IL-6, and TNF-α when peptide (Pep1) of SEQ ID NO: 1 is added by concentration after irradiation with ultraviolet B.

The peptide described in SEQ ID NO: 1 is shown in Table 1 below. SEQ ID NO: 2 is the sequence of a human telomerase full-length protein. SEQ ID NO: 1 is a peptide derived from telomerase and is a peptide composed of 16 amino acids. The “name” in Table 1 below is used to distinguish peptides. In another aspect of the present invention, the peptide of SEQ ID NO: 1 includes a "synthetic peptide" synthesized by selecting a peptide at a corresponding position among peptides included in telomerase.

One aspect of the present invention provides a polynucleotide encoding a peptide that is a fragment of SEQ ID NO: 1 or a peptide having at least 80% sequence homology to the peptide sequence. The polynucleotide can be used to mass-produce peptides that are fragments of SEQ ID NO: 1 or peptides having 80% or more sequence homology with the peptide sequences. For example, by culturing a vector containing a polynucleotide encoding one or more of the peptides of the fragments of SEQ ID NO: 1 into a host cell, the peptides of one or more of the peptides of the fragments of SEQ ID NO: 1 can be mass produced.

The peptides disclosed herein may include peptides that are fragments of SEQ ID NO: 1, and peptides having sequence homology of 80% or more, 85% or more, 90% or more, 95% or more, or 96% or more. In addition, the peptides disclosed herein are peptides that are fragments of SEQ ID NO: 1, 1 or more amino acids, 2 or more amino acids, 3 or more amino acids, 4 or more amino acids, 5 or more amino acids, 6 or more amino acids, or 7 or more amino acids It may include peptides with amino acid changes.

In one aspect of the invention, amino acid changes belong to properties that allow the physicochemical properties of the peptide to be altered. For example, amino acid changes can be performed, such as improving the thermal stability of the peptide, changing the substrate specificity, and changing the optimum pH.

As used herein, “amino acid” includes 22 standard amino acids that are naturally incorporated into peptides, as well as D-isomers and modified amino acids. Accordingly, in one aspect of the present invention, the peptide may be a peptide containing D-amino acid. Meanwhile, in another aspect of the present invention, the peptide may include a non-standard amino acid that has been post-translational modification. Examples of post-translational modifications include phosphorylation, glycosylation, acylation (e.g., acetylation, myristoylation and palmitoylation), alkylation ), Carboxylation, hydroxylation, glycation, biotinylation, ubiquitinylation, changes in chemical properties (e.g. beta-eliminated deimide , Deamidation) and structural changes (eg, formation of disulfide bridges). It also includes changes in amino acids, such as changes in amino groups, carboxyl groups or side chains, caused by chemical reactions that occur in the course of binding with crosslinkers to form peptide conjugates.

The peptides disclosed herein can be wild-type peptides that have been identified and isolated from intact sources. Meanwhile, the peptide disclosed herein may be an artificial variant comprising an amino acid sequence in which one or more amino acids have been substituted, deleted, and / or inserted compared to a peptide that is a fragment of SEQ ID NO: 1. Amino acid changes in wild-type polypeptides as well as in artificial variants include conservative amino acid substitutions that do not significantly affect the folding and / or activity of the protein. Examples of conservative substitutions are basic amino acids (arginine, lysine and histidine), acidic amino acids (glutamic acid and aspartic acid), polar amino acids (glutamine and asparagine), hydrophobic amino acids (leucine, isoleucine, valine and methionine), aromatic amino acids (phenylalanine, Tryptophan and tyrosine), and small amino acids (glycine, alanine, serine and threonine). In general, amino acid substitutions that do not alter specific activity are known in the art. The most common exchanges are Ala / Ser, Val / Ile, Asp / Glu, Thr / Ser, Ala / Gly, Ala / Thr, Ser / Asn, Ala / Val, Ser / Gly, Tyr / Phe, Ala / Pro, Lys / Arg, Asp / Asn, Leu / Ile, Leu / Val, Ala / Glu, and Asp / Gly, and vice versa.

In addition, another aspect of the present invention provides a composition comprising a peptide or a fragment thereof having 80% or more sequence homology with a peptide or a peptide derived from the human protein as described above as an active ingredient.

Skin cells exhibit a cell damage response by inducing various biochemical changes in the cells by stimulation of cell damage such as ultraviolet rays, environmental pollutants, and rapid temperature changes applied from the outside. When the cell membrane of skin cells is continuously damaged by free radicals or other radicals, cross-linkage of proteins or lipoproteins increases or decomposes, thereby increasing the amount of lipid peroxide. Therefore, the permeability of the cell membrane is changed and the ion balance in the cell is broken, and this change prevents the discharge of metabolic debris in the cell and also decreases the function of the cell to detoxify the metabolic debris. And, if the colloid density increases due to the increase in the concentration of potassium in the cell, the synthesis of mRNA or protein is hindered, and the ability to repair cell damage is further reduced.

If the cell-level change continues as described above, the tissue structure of the skin tissue loses its regularity, and at the same time, the individual cells are relatively large, and the total cell number is decreased. In addition, local scars appear on the dermis, and the thickness of the dermis is reduced due to the reduction of collagen fibers or elastic fibers. The crosslinking between collagen fibers also increases, and the fine structure of the elastic fibers is also damaged, resulting in a decrease in elasticity of the skin as a whole. That is, oxidative damage of skin cells caused by an external stimulus ultimately promotes aging of the skin.

Substances causing such oxidative cell damage include hydrogen peroxide (H ₂ O ₂ ), superoxide anion, and hydroxyl radical generated by oxidative stress. To eliminate endotoxins, our bodies are equipped with endogenous antioxidant systems such as glutathione and superoxide dismutase (SOD). However, when the metabolic activity in the cell is excessively increased, or when the body is exposed to an exogenous stress such as infection, excessive exercise, radiation, or a compound, the endogenous antioxidant capacity may be exceeded. At this time, cell damage caused by free radicals may occur. .

Accordingly, one aspect of the present invention is a peptide derived from a human protein, by providing a composition comprising a peptide that is a fragment of SEQ ID NO: 1 or a peptide having 80% or more sequence homology with the peptide sequence or a fragment thereof as an active ingredient, skin By increasing the endogenous antioxidant power of the cell itself, that is, the physiological reducing power of the cell, it is possible to suppress cell damage from stimulation such as ultraviolet light. Therefore, when applied or administered to the skin, the peptide can protect the skin from irritation such as ultraviolet rays by preventing intracellular toxicity and prevent or treat skin damage.

The composition according to one aspect of the present invention is a peptide of the fragments of SEQ ID NO: 1 or a peptide having a sequence homology of 80% or more with the peptide sequence is 0.1 μg / mg to 1 mg / mg, specifically 1 μg / mg to 0.5 mg / Mg, more specifically, 10 μg / mg to 0.1 mg / mg. When included in the above range, it is not only suitable to exhibit the intended effect of the present invention, but also satisfies both the stability and safety of the composition, and it may be appropriate to include the above range in terms of cost effectiveness.

The composition according to one aspect of the present invention can be applied to all animals including humans, dogs, chickens, pigs, cows, sheep, guinea pigs or monkeys.

The pharmaceutical composition according to one aspect of the present invention may be administered orally, rectal, transdermal, intravenous, intramuscular, intraperitoneal, intramedullary, intrathecal or subcutaneous.

Formulations for oral administration may be tablets, pills, soft or hard capsules, granules, powders, liquids or emulsions, but are not limited thereto. Formulations for parenteral administration may be, but are not limited to, injections, drops, lotions, ointments, gels, creams, suspensions, emulsions, suppositories, patches or sprays.

The pharmaceutical composition according to one aspect of the present invention may include additives such as diluents, excipients, lubricants, binders, disintegrants, buffers, dispersants, surfactants, colorants, flavors or sweeteners, if necessary. Pharmaceutical compositions according to one aspect of the present invention can be prepared by conventional methods in the art.

The active ingredient of the pharmaceutical composition according to one aspect of the present invention will vary depending on the age, gender, weight, pathology and severity of the subject to be administered, the route of administration or the judgment of the prescriber. Determination of the application amount based on these factors is within the level of those skilled in the art, the daily dosage of which is, for example, 0.1 μg / kg / day to 1 g / kg / day, specifically 1 μg / kg / day to 10 mg / kg / Day, more specifically 10 μg / kg / day to 1 mg / kg / day, and more specifically 50 μg / kg / day to 100 μg / kg / day, but is not limited thereto. The pharmaceutical composition according to one aspect of the present invention may be administered once to three times a day, but is not limited thereto.

According to the pharmaceutical composition according to an aspect of the present invention, it is possible to prevent or improve various symptoms or diseases as ultraviolet rays are irradiated to the skin. For example, sunburn caused by UV-induced skin irritation, erythema, edema, pigmentation, skin irritation, skin exfoliation, as well as photosensitization phenomena such as photoallergy, phototoxicity, photoaging or melanoma as a chronic reaction. It can prevent or improve the occurrence of skin cancer.

The cosmetic composition according to one aspect of the present invention may be provided in any formulation suitable for topical application. For example, it may be provided in the form of a solution, an emulsion obtained by dispersing an oil phase in an aqueous phase, an emulsion obtained by dispersing an oil phase in an oil phase, suspension, solid, gel, powder, paste, foam or aerosol. Such formulations can be prepared according to conventional methods in the art.

In addition, the cosmetic composition according to an aspect of the present invention may be provided as an injection liquid formulation. The cosmetic composition of this injection solution formulation is a syringe with a single needle, a syringe with a plurality of needles, a patch, a micro needle or a microjet method, or a high-speed injection or injection solution through a shock wave caused by applying a laser beam to an aluminum foil. It can be injected into the skin through a variety of delivery mechanisms, such as a mechanism for spraying. According to the method using the laser, since an injection needle is not used, it is possible to prevent pain at the time of injection and wound due to the use of an injection needle. As described above, according to the injection solution formulation, the active ingredient included in the cosmetic composition can be directly delivered to the target site such as the skin, thereby maximizing the effect. In addition, according to the method using a laser, since an injection needle is not used, pain during injection and a wound due to the use of an injection needle can be prevented.

The cosmetic composition according to an aspect of the present invention may include other ingredients that can give a synergistic effect to the main effect, within a range that does not impair the main effect. In addition, the cosmetic composition according to an aspect of the present invention is a moisturizer, emollient, surfactant, ultraviolet absorber, preservative, disinfectant, antioxidant, pH adjusting agent, organic or inorganic pigment, fragrance, cooling agent, or limiting agent It can contain. The blending amount of the components can be easily selected by those skilled in the art within a range that does not impair the object and effect of the present invention, the blending amount is 0.01 to 5% by weight based on the total weight of the cosmetic composition, specifically 0.01 to 3% by weight You can.

The formulation of the food composition according to one aspect of the present invention is not particularly limited, but may be formulated into, for example, tablets, granules, powders, liquids, solid preparations, and the like. Each formulation can be formulated by appropriately selecting the ingredients commonly used in the field other than the active ingredient according to the formulation or purpose of use without difficulty, and synergistic effects may occur when applied simultaneously with other raw materials.

Determination of the dosage of the active ingredient is within the level of those skilled in the art, the daily dosage of which is, for example, specifically 1 μg / kg / day to 10 mg / kg / day, more specifically 10 μg / kg / day To 1 mg / kg / day, more specifically, 50 µg / kg / day to 100 µg / kg / day, but is not limited thereto, and various factors such as age, health condition, and complications of the subject to be administered May vary.

Ultraviolet rays synthesize beneficial vitamin D in the body and act as a bactericidal agent, while also producing skin aging, skin cancer, dryness, dermatitis, fine lines, blemishes, and freckles. Ultraviolet (UV) is divided into three types, A, B, and C, depending on the wavelength, of which UVC is blocked in the ozone layer, and UVA and UVB affect the skin. UVA accounts for more than 90% of ultraviolet rays and is considered a major cause of skin aging. It exists throughout the four seasons, from sunrise to sunset. Even on cloudy and cloudy days, it cannot be avoided, and the glass also penetrates. UVB increases in the summer and has a shorter wavelength than UVA, so it does not penetrate deep into the skin, but excessive exposure can cause sunburn, erythema, blisters, burns, and inflammation, which can cause skin aging.

Hereinafter, the composition and effects of the present invention will be described in more detail by confirming the effect of the peptide PEP 1 according to the present invention on UVA and UVB by Examples and Experimental Examples. However, the following examples and experimental examples are provided for illustrative purposes only to aid understanding of the present invention, and the scope and scope of the present invention are not limited thereto.

Example  1: Synthesis of peptides

The peptides disclosed herein were prepared according to a conventionally known solid-phase peptide synthesis method. Specifically, peptides were synthesized by coupling amino acids one by one from the C-terminal through Fmoc solid phase peptide synthesis (SPPS) using ASP48S (Peptron, Inc., Daejeon, Korea). As follows, the first amino acid at the C-terminal of the peptides was used. For example:

NH ₂ -Lys (Boc) -2-chloro-Trityl Resin

NH ₂ -Ala-2-chloro-Trityl Resin

NH ₂ -Arg (Pbf) -2-chloro-Trityl Resin

All amino acid raw materials used for peptide synthesis are Trt, Boc, t-Bu (t-butylester), Pbf (2,2,4,6, where N-term is protected by Fmoc and all residues are removed from the acid. 7-pentamethyl dihydro-benzofuran-5-sulfonyl). For example:

Fmoc-Ala-OH, Fmoc-Arg (Pbf) -OH, Fmoc-Glu (OtBu) -OH, Fmoc-Pro-OH, Fmoc-Leu-OH, Fmoc-Ile-OH, Fmoc-Phe-OH, Fmoc- Ser (tBu) -OH, Fmoc-Thr (tBu) -OH, Fmoc-Lys (Boc) -OH, Fmoc-Gln (Trt) -OH, Fmoc-Trp (Boc) -OH, Fmoc-Met-OH, Fmoc -Asn (Trt) -OH, Fmoc-Tyr (tBu) -OH, Fmoc-Ahx-OH, Trt-Mercaptoacetic acid.

HBTU [2- (1H-Benzotriazole-1-yl) -1,1,3,3-tetamethylaminium hexafluorophosphate] / HOBt [N-Hydroxxybenzotriazole] / NMM [4-Methylmorpholine] is used as the coupling reagent. Did. Fmoc removal was performed using piperidine in DMF in 20% of DMF. Cleavage Cocktail [TFA (trifluoroacetic acid) / TIS (triisopropylsilane) / EDT (ethanedithiol) / H ₂ O = 92.5 / 2.5 / 2.5 / 2.5] is used for separating the synthesized peptide from Resin and removing the protecting group of the residue. Did.

Each peptide was synthesized by reacting the corresponding amino acids therein, washing with a solvent, and repeating the deprotection process using the state in which the amino acid protecting group-bound starting amino acid is bound to the solid support. The synthesized peptide was removed from the resin and then purified by HPLC. Synthesis was confirmed by MS and lyophilized.

The specific process will be described using Pep 1 of SEQ ID NO: 1 as an example.

1) Coupling

NH ₂ -Lys (Boc) -2-chloro-Trityl Resin protected amino acid (8 eq) and coupling reagent HBTU (8 eq) / HOBt (8 eq) / NMM (16 eq) dissolved in DMF and added , Reacted at room temperature for 2 hours, washed with DMF, MeOH, and DMF.

2) Fmoc deprotection

Piperidine in DMF was added in 20% of DMF, reacted twice at room temperature for 5 minutes, and washed in the order of DMF, MeOH, and DMF.

3) The reaction of 1 and 2 is repeated to the peptide base skeleton NH ₂ -E (OtBu) -AR (Pbf) -PALLT (tBu) -S (tBu) -R (Pbf) LR (Pbf) -FIPK (Boc) -2-chloro-Trityl Resin).

4) Cleavagge: Cleavage Cocktail was added to the synthesized peptide Resin to separate the peptide from Resin.

5) After adding cooling diethyl ether to the obtained mixture, the obtained peptide is precipitated by centrifugation.

6) After purification by Prep-HPLC, molecular weight was confirmed by LC / MS and frozen to prepare powder.

Example  2: Peptide of SEQ ID NO: 1 Pep1 ) To test the effect of alleviating cytotoxicity by ultraviolet rays

1) Cell culture

Human dermal fibroblasts were purchased from Gibco. The purchased human dermal fibroblasts were cultured under Medium 5 medium by adding Low Serum Growth Supplement (LSGS) at 37 ° C. under 5% CO ₂ conditions and subcultured by trypsinization to obtain 3-5th generation cells.

2) Effect of alleviating cytotoxicity by UVA irradiation

Human dermal fibroblasts cultured as above were put in 1 ⅹ 10 ⁴ / well in a 96-well plate and cultured for 16-18 hours. After the culture medium was removed before UVA irradiation, 4.5 J / cm 2 UVA was irradiated after washing with a phosphate buffer solution (PBS). After UVA irradiation, the peptide (Pep1) of SEQ ID NO: 1 according to one aspect of the present invention was treated with medium (10, 100, 500 µg / ml) according to one aspect of the present invention without serum, and cultured for 24 hours.

After 24 hours, 10 μl of the MTT solution (3- (4,5-Dimethylthiazol-2-yl) -2,5-diphenyltetrazoliumbromide; 5 mg / ml) was added and 37 ° C and 5% CO ₂ conditions for 2 hours Cultured under. The medium was removed, 100 μl of DMSO (dimethylsulfoxide) was added, shaken at room temperature for 10 minutes, and absorbance was measured using a microplate reader at 570 nm. The results of calculating the survival rate of cells through the measured absorbance are shown in FIG. 1. At this time, the survival rate of the cells was calculated by Equation 1 below.

Blank: Absorbance at 570 nm of wells that developed only the cell culture medium

treated : 570nm absorbance of the wells that developed and reacted the wells treated with the sample (Pep1)

untreated: 570nm absorbance of the wells that developed and reacted wells not treated with the sample (Pep1)

As shown in Figure 1, when the survival rate of the cells after irradiation with ultraviolet light is not irradiated with ultraviolet light, and when the peptide of SEQ ID NO: 1 according to an aspect of the present invention is not added to 100%, when irradiated with ultraviolet light There was a decrease of 80%. In addition, when the peptide of SEQ ID NO: 1 was added at a concentration of 10, 100, 500 µg / ml after UV irradiation, it was found that the survival rate of the cells increased as the concentration increased, and in particular, the concentration of the peptide was 100 µg / ml. When added as, the survival rate of the cells was almost 100%, and when the peptide was added at a concentration of 500 µg / ml, the survival rate of the cells was higher than that without irradiation with ultraviolet rays. This means that the survival rate of cells is increased accordingly by alleviating the cytotoxicity caused by ultraviolet irradiation of the peptide according to one aspect of the present invention. Therefore, it can be seen through this that the peptide according to one aspect of the present invention can prevent or treat skin damage caused by ultraviolet rays.

Example  3: Peptide of SEQ ID NO: 1 Pep1 ) Inhibitory effect of inflammatory cytokine expression by ultraviolet irradiation

1) Cell culture

Normal human epidermal keratinocytes were purchased from Gibco. The purchased normal human epithelial keratinocytes were added to Keratinocyte-SFM medium by adding Bovine Pituitary Extract (BPE) and EGF (Epidermal Growth Factor, Human Recombinant), and cultured under 37 ° C and 5% CO ₂ conditions, followed by trypsinization. Passage cultures yielded 3 to 5 generation cells.

2) Inhibitory effect of inflammatory cytokines by UVB irradiation

The human epithelial keratinocytes cultured as above were put in a 2 ⅹ 10 ⁵ / well in a 12-well plate and cultured for 16-18 hours. After removing the culture medium before UVB irradiation, 25 mJ / cm 2 UVB was irradiated after washing with a phosphate buffer solution (PBS). After UVB irradiation, BPE (Bovine Pituitary Extract) and EGF (Epidermal Growth Factor, Human Recombinant) are not added to the Keratinocyte-SFM medium according to one aspect of the present invention. , 100, 500, 1000 μg / ml) and cultured for 24 hours.

After 24 hours, the culture supernatant was collected to quantify IL-1α, IL-6, and TNF-α to determine the inhibitory effect of inflammatory cytokine expression. The amount of inflammatory cytokines was quantified using ELISA, and the production rate of inflammatory cytokines was calculated by Equation 2.

B0: Inflammatory cytokine production in wells that did not irradiate with ultraviolet light and did not process the sample (Pep1)

Bt: Inflammatory cytokine production in wells that were not irradiated with ultraviolet light and treated with the sample (Pep1)

St: Inflammatory cytokine production in wells treated with UV and sample (Pep1)

As shown in FIG. 2, IL-1α was 38.1%, 32.9%, and 27.2% when peptide (Pep1) of SEQ ID NO: 1 was added by concentration after irradiation with ultraviolet B. 12.1%, 30.7%, IL-6 inhibited 55.6%, 51.6%, 34.4%, 33.5%, 36.8%, and TNF-α was 20.7%, 20.3%, 16.1%, 20.4%, 32.4%. Suppressed. It can be seen that these results effectively prevent the occurrence of inflammation caused by ultraviolet rays even at a low concentration of peptide (Pep1) treatment.

Accordingly, it can be seen that according to the peptide according to one aspect of the present invention, it is possible to prevent or treat skin damage by suppressing an inflammatory reaction caused by ultraviolet rays.

<110> KAEL-GemVax Co., Ltd.          KIM, SANGJAE <120> Composition for preventing or treating skin damages caused by          ultraviolet rays <130> 13P540IND <150> KR 10-2012-0145501 <151> 2012-12-13 <160> 2 <170> KopatentIn 2.0 <210> 1 <211> 16 <212> PRT <213> Homo sapiens <400> 1 Glu Ala Arg Pro Ala Leu Leu Thr Ser Arg Leu Arg Phe Ile Pro Lys   1 5 10 15 <210> 2 <211> 1132 <212> PRT <213> Homo sapiens <400> 2 Met Pro Arg Ala Pro Arg Cys Arg Ala Val Arg Ser Leu Leu Arg Ser   1 5 10 15 His Tyr Arg Glu Val Leu Pro Leu Ala Thr Phe Val Arg Arg Leu Gly              20 25 30 Pro Gln Gly Trp Arg Leu Val Gln Arg Gly Asp Pro Ala Ala Phe Arg          35 40 45 Ala Leu Val Ala Gln Cys Leu Val Cys Val Pro Trp Asp Ala Arg Pro      50 55 60 Pro Pro Ala Ala Pro Ser Phe Arg Gln Val Ser Cys Leu Lys Glu Leu  65 70 75 80 Val Ala Arg Val Leu Gln Arg Leu Cys Glu Arg Gly Ala Lys Asn Val                  85 90 95 Leu Ala Phe Gly Phe Ala Leu Leu Asp Gly Ala Arg Gly Gly Pro Pro             100 105 110 Glu Ala Phe Thr Thr Ser Val Arg Ser Tyr Leu Pro Asn Thr Val Thr         115 120 125 Asp Ala Leu Arg Gly Ser Gly Ala Trp Gly Leu Leu Leu Arg Arg Val     130 135 140 Gly Asp Asp Val Leu Val His Leu Leu Ala Arg Cys Ala Leu Phe Val 145 150 155 160 Leu Val Ala Pro Ser Cys Ala Tyr Gln Val Cys Gly Pro Pro Leu Tyr                 165 170 175 Gln Leu Gly Ala Ala Thr Gln Ala Arg Pro Pro Pro His Ala Ser Gly             180 185 190 Pro Arg Arg Arg Leu Gly Cys Glu Arg Ala Trp Asn His Ser Val Arg         195 200 205 Glu Ala Gly Val Pro Leu Gly Leu Pro Ala Pro Gly Ala Arg Arg Arg     210 215 220 Gly Gly Ser Ala Ser Arg Ser Leu Pro Leu Pro Lys Arg Pro Arg Arg 225 230 235 240 Gly Ala Ala Pro Glu Pro Glu Arg Thr Pro Val Gly Gln Gly Ser Trp                 245 250 255 Ala His Pro Gly Arg Thr Arg Gly Pro Ser Asp Arg Gly Phe Cys Val             260 265 270 Val Ser Pro Ala Arg Pro Ala Glu Glu Ala Thr Ser Leu Glu Gly Ala         275 280 285 Leu Ser Gly Thr Arg His Ser His Pro Ser Val Gly Arg Gln His His     290 295 300 Ala Gly Pro Pro Ser Thr Ser Arg Pro Pro Arg Pro Trp Asp Thr Pro 305 310 315 320 Cys Pro Pro Val Tyr Ala Glu Thr Lys His Phe Leu Tyr Ser Ser Gly                 325 330 335 Asp Lys Glu Gln Leu Arg Pro Ser Phe Leu Leu Ser Ser Leu Arg Pro             340 345 350 Ser Leu Thr Gly Ala Arg Arg Leu Val Glu Thr Ile Phe Leu Gly Ser         355 360 365 Arg Pro Trp Met Pro Gly Thr Pro Arg Arg Leu Pro Arg Leu Pro Gln     370 375 380 Arg Tyr Trp Gln Met Arg Pro Leu Phe Leu Glu Leu Leu Gly Asn His 385 390 395 400 Ala Gln Cys Pro Tyr Gly Val Leu Leu Lys Thr His Cys Pro Leu Arg                 405 410 415 Ala Ala Val Thr Pro Ala Ala Gly Val Cys Ala Arg Glu Lys Pro Gln             420 425 430 Gly Ser Val Ala Ala Pro Glu Glu Glu Asp Thr Asp Pro Arg Arg Leu         435 440 445 Val Gln Leu Leu Arg Gln His Ser Ser Pro Trp Gln Val Tyr Gly Phe     450 455 460 Val Arg Ala Cys Leu Arg Arg Leu Val Pro Pro Gly Leu Trp Gly Ser 465 470 475 480 Arg His Asn Glu Arg Arg Phe Leu Arg Asn Thr Lys Lys Phe Ile Ser                 485 490 495 Leu Gly Lys His Ala Lys Leu Ser Leu Gln Glu Leu Thr Trp Lys Met             500 505 510 Ser Val Arg Asp Cys Ala Trp Leu Arg Arg Ser Pro Gly Val Gly Cys         515 520 525 Val Pro Ala Ala Glu His Arg Leu Arg Glu Glu Ile Leu Ala Lys Phe     530 535 540 Leu His Trp Leu Met Ser Val Tyr Val Val Glu Leu Leu Arg Ser Phe 545 550 555 560 Phe Tyr Val Thr Glu Thr Thr Phe Gln Lys Asn Arg Leu Phe Phe Tyr                 565 570 575 Arg Lys Ser Val Trp Ser Lys Leu Gln Ser Ile Gly Ile Arg Gln His             580 585 590 Leu Lys Arg Val Gln Leu Arg Glu Leu Ser Glu Ala Glu Val Arg Gln         595 600 605 His Arg Glu Ala Arg Pro Ala Leu Leu Thr Ser Arg Leu Arg Phe Ile     610 615 620 Pro Lys Pro Asp Gly Leu Arg Pro Ile Val Asn Met Asp Tyr Val Val 625 630 635 640 Gly Ala Arg Thr Phe Arg Arg Glu Lys Arg Ala Glu Arg Leu Thr Ser                 645 650 655 Arg Val Lys Ala Leu Phe Ser Val Leu Asn Tyr Glu Arg Ala Arg Arg             660 665 670 Pro Gly Leu Leu Gly Ala Ser Val Leu Gly Leu Asp Asp Ile His Arg         675 680 685 Ala Trp Arg Thr Phe Val Leu Arg Val Arg Ala Gln Asp Pro Pro Pro     690 695 700 Glu Leu Tyr Phe Val Lys Val Asp Val Thr Gly Ala Tyr Asp Thr Ile 705 710 715 720 Pro Gln Asp Arg Leu Thr Glu Val Ile Ala Ser Ile Ile Lys Pro Gln                 725 730 735 Asn Thr Tyr Cys Val Arg Arg Tyr Ala Val Val Gln Lys Ala Ala His             740 745 750 Gly His Val Arg Lys Ala Phe Lys Ser His Val Ser Thr Leu Thr Asp         755 760 765 Leu Gln Pro Tyr Met Arg Gln Phe Val Ala His Leu Gln Glu Thr Ser     770 775 780 Pro Leu Arg Asp Ala Val Val Ile Glu Gln Ser Ser Ser Leu Asn Glu 785 790 795 800 Ala Ser Ser Gly Leu Phe Asp Val Phe Leu Arg Phe Met Cys His His                 805 810 815 Ala Val Arg Ile Arg Gly Lys Ser Tyr Val Gln Cys Gln Gly Ile Pro             820 825 830 Gln Gly Ser Ile Leu Ser Thr Leu Leu Cys Ser Leu Cys Tyr Gly Asp         835 840 845 Met Glu Asn Lys Leu Phe Ala Gly Ile Arg Arg Asp Gly Leu Leu Leu     850 855 860 Arg Leu Val Asp Asp Phe Leu Leu Val Thr Pro His Leu Thr His Ala 865 870 875 880 Lys Thr Phe Leu Arg Thr Leu Val Arg Gly Val Pro Glu Tyr Gly Cys                 885 890 895 Val Val Asn Leu Arg Lys Thr Val Val Asn Phe Pro Val Glu Asp Glu             900 905 910 Ala Leu Gly Gly Thr Ala Phe Val Gln Met Pro Ala His Gly Leu Phe         915 920 925 Pro Trp Cys Gly Leu Leu Leu Asp Thr Arg Thr Leu Glu Val Gln Ser     930 935 940 Asp Tyr Ser Ser Tyr Ala Arg Thr Ser Ile Arg Ala Ser Leu Thr Phe 945 950 955 960 Asn Arg Gly Phe Lys Ala Gly Arg Asn Met Arg Arg Lys Leu Phe Gly                 965 970 975 Val Leu Arg Leu Lys Cys His Ser Leu Phe Leu Asp Leu Gln Val Asn             980 985 990 Ser Leu Gln Thr Val Cys Thr Asn Ile Tyr Lys Ile Leu Leu Leu Gln         995 1000 1005 Ala Tyr Arg Phe His Ala Cys Val Leu Gln Leu Pro Phe His Gln Gln    1010 1015 1020 Val Trp Lys Asn Pro Thr Phe Phe Leu Arg Val Ile Ser Asp Thr Ala 1025 1030 1035 1040 Ser Leu Cys Tyr Ser Ile Leu Lys Ala Lys Asn Ala Gly Met Ser Leu                1045 1050 1055 Gly Ala Lys Gly Ala Ala Gly Pro Leu Pro Ser Glu Ala Val Gln Trp            1060 1065 1070 Leu Cys His Gln Ala Phe Leu Leu Lys Leu Thr Arg His Arg Val Thr        1075 1080 1085 Tyr Val Pro Leu Leu Gly Ser Leu Arg Thr Ala Gln Thr Gln Leu Ser    1090 1095 1100 Arg Lys Leu Pro Gly Thr Thr Leu Thr Ala Leu Glu Ala Ala Ala Asn 1105 1110 1115 1120 Pro Ala Leu Pro Ser Asp Phe Lys Thr Ile Leu Asp                1125 1130

Claims (8)

As an active ingredient,
As a pharmaceutical composition for preventing or treating skin damage caused by ultraviolet rays comprising a peptide consisting of SEQ ID NO: 1,
The skin damage caused by the ultraviolet rays is any one selected from the group consisting of sunburn, erythema, edema, pigmentation, skin inflammation, skin keratinization, photoallergy, phototoxicity, photosensitization, and photoaging. According to claim 1,
The active ingredient is a pharmaceutical composition for preventing or treating skin damage caused by ultraviolet rays, which performs a function of alleviating cytotoxicity by ultraviolet rays. According to claim 2,
The ultraviolet rays are UVA, a pharmaceutical composition for preventing or treating skin damage caused by ultraviolet rays. According to claim 2,
The ultraviolet light is UVB, a pharmaceutical composition for preventing or treating skin damage caused by ultraviolet light. As an active ingredient,
As a cosmetic composition for preventing or improving skin damage caused by ultraviolet rays comprising a peptide consisting of SEQ ID NO: 1,
The skin damage caused by ultraviolet rays is any one selected from the group consisting of sunburn, erythema, edema, pigmentation, skin inflammation, skin keratinization, photoallergy, phototoxicity, photosensitization, and photoaging. As an active ingredient,
As a health food composition for preventing or improving skin damage caused by ultraviolet rays comprising a peptide consisting of SEQ ID NO: 1,
The skin damage caused by ultraviolet rays is any one selected from the group consisting of sunburn, erythema, edema, pigmentation, skin inflammation, skin keratinization, photoallergy, phototoxicity, photosensitization, and photoaging.
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