CN114432284A - Application of adipic acid in preparation of product for resisting skin photodamage - Google Patents
Application of adipic acid in preparation of product for resisting skin photodamage Download PDFInfo
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- CN114432284A CN114432284A CN202210260369.0A CN202210260369A CN114432284A CN 114432284 A CN114432284 A CN 114432284A CN 202210260369 A CN202210260369 A CN 202210260369A CN 114432284 A CN114432284 A CN 114432284A
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Images
Classifications
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/185—Acids; Anhydrides, halides or salts thereof, e.g. sulfur acids, imidic, hydrazonic or hydroximic acids
- A61K31/19—Carboxylic acids, e.g. valproic acid
- A61K31/194—Carboxylic acids, e.g. valproic acid having two or more carboxyl groups, e.g. succinic, maleic or phthalic acid
-
- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23L—FOODS, FOODSTUFFS, OR NON-ALCOHOLIC BEVERAGES, NOT COVERED BY SUBCLASSES A21D OR A23B-A23J; THEIR PREPARATION OR TREATMENT, e.g. COOKING, MODIFICATION OF NUTRITIVE QUALITIES, PHYSICAL TREATMENT; PRESERVATION OF FOODS OR FOODSTUFFS, IN GENERAL
- A23L33/00—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof
- A23L33/10—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof using additives
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K8/00—Cosmetics or similar toiletry preparations
- A61K8/18—Cosmetics or similar toiletry preparations characterised by the composition
- A61K8/30—Cosmetics or similar toiletry preparations characterised by the composition containing organic compounds
- A61K8/33—Cosmetics or similar toiletry preparations characterised by the composition containing organic compounds containing oxygen
- A61K8/36—Carboxylic acids; Salts or anhydrides thereof
- A61K8/362—Polycarboxylic acids
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P17/00—Drugs for dermatological disorders
- A61P17/16—Emollients or protectives, e.g. against radiation
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61Q—SPECIFIC USE OF COSMETICS OR SIMILAR TOILETRY PREPARATIONS
- A61Q19/00—Preparations for care of the skin
- A61Q19/08—Anti-ageing preparations
-
- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23V—INDEXING SCHEME RELATING TO FOODS, FOODSTUFFS OR NON-ALCOHOLIC BEVERAGES AND LACTIC OR PROPIONIC ACID BACTERIA USED IN FOODSTUFFS OR FOOD PREPARATION
- A23V2002/00—Food compositions, function of food ingredients or processes for food or foodstuffs
Abstract
The invention belongs to the technical field of biomedicine, and particularly discloses application of adipic acid in preparation of a product for resisting skin photodamage. The experimental result proves that the adipic acid can improve the oxidative damage of the UVB-induced cells by reducing the expression levels of ROS, MDA and SOD in the UVB-induced oxidative damage cells and reducing the relative expression amounts of MMP-1, MMP-3 and MMP-9 and the expression amount of MMP-1 protein.
Description
Technical Field
The invention belongs to the technical field of biomedicine, and particularly discloses application of adipic acid in preparation of a product for resisting skin photodamage.
Background
Skin is the largest organ of the human body, and skin aging is one of the main manifestations of aging of the body. Photoaging of skin by ultraviolet rays is the most critical factor causing aging damage of skin. Photoaged skin is characterized by rough, thickened and dry exposed areas of the skin, loose skin, increased wrinkles, local hyperpigmentation or telangiectasia, and may even present with various benign or malignant tumors (e.g., solar keratosis, squamous cell carcinoma, malignant melanoma, etc.).
The skin is the first defense barrier of the human body, covering the whole body. Skin disease treatmentIs the largest organ, accounting for about 16% of the human body. The skin area of an adult is about 1.2-2.0m2. The skin is directly contacted with the external environment, and has the functions of sensing external stimulation, regulating body temperature, excreting metabolites, protecting the body from physical, mechanical and chemical damages and invasion of pathogenic microorganisms, and the like. The skin consists of three parts, namely epidermis, dermis and subcutaneous tissue.
Ultraviolet light is the main cause of skin photoaging. Sunlight consists of 53% infrared, 44% visible and 3% UV. UV is electromagnetic radiation having a wavelength of 100-400 nm. According to the different radiation wavelengths, UV can be divided into long-wave UV (UVA, wavelength is 315-400nm), medium-wave UV (UVB, wavelength is 280-315nm) and short-wave UV (UVC, wavelength is 200-280 nm). Proper ultraviolet radiation can kill microorganisms, regulate nerve, endocrine, digestive, respiratory and immune systems, and promote the synthesis of vitamin D. But prolonged exposure to low or transient exposure to high doses of uv radiation can cause damage to the human eye, skin, immune system, etc. UVA and UVB are the main light sources responsible for skin aging. UVA has a strong capacity to cause the production of cellular free radicals and lipid peroxidation, and can affect collagen fibers and elastic fibers in dermal tissue. UVA has strong penetrating power, the influence can reach the deep dermis, and although the influence has no direct influence on DNA damage, the UVA can indirectly generate Reactive Oxygen Species (ROS), so that the DNA is oxidized and damaged. UVB mainly causes skin epidermal layer and dermal superficial layer lesion, and UVB can be absorbed by protein and DNA in cells, causing cell damage and mutation. Studies have shown that over 80% of facial skin aging is caused by uv irradiation. Macroscopic features of skin photoaging include wrinkle formation, rough texture, pigmentation, loss of skin elasticity, and the like; histological and ultrastructural studies have shown photoaging skin epidermal hyperplasia, collagen fiber damage disorders, massive accumulation of abnormal elastic substances in the skin connective tissue, etc.
Adipic acid (Adipic acid), also known as Adipic acid, is an important organic dibasic acid, can undergo salt formation, esterification, amidation, and the like, and can be polycondensed with diamine or diol to form high-molecular polymers, and the like. Adipic acid is a dicarboxylic acid with important industrial significance, and plays an important role in chemical production, organic synthesis industry, medicine, lubricant manufacturing and other aspects. However, the application of adipic acid in improving UVB-induced cell oxidative damage and resisting skin photoaging is not reported.
Disclosure of Invention
In view of the above technical problems, the present invention provides the following technical solutions:
the invention provides application of adipic acid in preparing products for resisting skin photodamage.
Preferably, the adipic acid is capable of ameliorating UVB-induced oxidative damage of cells.
Preferably, the adipic acid is capable of down-regulating the expression levels of ROS, MDA and SOD.
Preferably, the adipic acid is capable of down-regulating the relative expression levels of MMP-1, MMP-3 and MMP-9.
Preferably, the adipic acid is capable of down-regulating the expression level of MMP-1 protein.
The invention also provides a pharmaceutical composition for preventing and/or treating skin photodamage, which comprises the adipic acid or the salt thereof and pharmaceutically acceptable auxiliary materials or carriers.
The invention also provides a health-care food composition for improving skin photoaging, which comprises the adipic acid or the salt thereof and food acceptable auxiliary materials.
Preferably, the health food composition can improve skin wrinkles, enhance skin elasticity, refine skin, and reduce pigmentation.
The present invention also provides a cosmetic composition comprising adipic acid or a salt thereof as defined in any of the preceding claims, and at least one cosmetically acceptable adjuvant or carrier.
Preferably, the cosmetic composition can improve skin photoaging and skin aging caused by ultraviolet irradiation.
Compared with the prior art, the invention has the beneficial effects that:
the invention provides application of adipic acid in preparing products for resisting skin photodamage. Cell tests prove that: the adipic acid can reduce the expression levels of ROS, MDA and SOD in oxidative damage cells induced by UVB, reduce the relative expression amounts of MMP-1, MMP-3 and MMP-9 and the expression amount of MMP-1 protein to improve the oxidative damage of the cells induced by UVB and improve the symptoms of wrinkle formation, rough texture, pigmentation, skin elasticity loss and the like caused by ultraviolet irradiation.
Drawings
FIG. 1 is a graph of the effect of UVB radiation dose on cell viability;
FIG. 2 is a graph of the effect of different concentrations of adipic acid on cell viability;
FIG. 3 is the effect on ROS accumulation in UVB-induced oxidative damage cells; in comparison with the UVB5 group,****P<0.0001；
FIG. 4 is a graph of the effect on MDA accumulation in UVB-induced oxidative damage cells; in comparison with the UVB5 group,***P<0.001；
FIG. 5 is a graph of the effect on SOD accumulation in UVB-induced oxidative damage cells; in comparison with the UVB5 group,***P<0.001；
FIG. 6 is a graph of the effect on the relative expression of MMP-1 in UVB-induced oxidative damage cells; in comparison with the UVB5 group,*P<0.05；
FIG. 7 is a graph of the effect on the relative expression of MMP-3 in UVB-induced oxidative damage cells; in comparison with the UVB5 group,**P<0.01，****P<0.0001；
FIG. 8 is a graph of the effect on the relative expression of MMP-9 in UVB-induced oxidative damage cells; in comparison with the UVB5 group,***P<0.001；
FIG. 9 is a graph showing the effect on the expression level of MMP-1 protein in UVB-induced oxidative damage cells, compared with UVB5 group,**P<0.01，****P<0.0001。
Detailed Description
The present invention is further illustrated by the following examples and accompanying drawings, which are provided for illustrative purposes only and are not intended to limit the scope of the present invention.
The invention provides application of adipic acid in preparing products for resisting skin photodamage.
The adipic acid has a structural formula shown as formula I, and a molecular formula of C6H10O4。
The method for obtaining adipic acid is not particularly limited, and may be synthesized by a known production method or may be commercially available.
The adipic acid can reduce the expression levels of ROS, MDA and SOD in oxidative damage cells induced by UVB, reduce the relative expression levels of MMP-1, MMP-3 and MMP-9, and reduce the expression level of MMP-1 protein to improve the oxidative damage of the cells induced by UVB.
The following description will be given with reference to specific examples.
Example 1
Inducing photoaging damage of HaCaT cells
HaCaT cells were seeded in 96-well plates and 0, 3, 5, 7, 10, 20, 30mJ/cm were administered when grown to a density of 50%2After culturing for 24 hours, the cell survival rate under different ultraviolet irradiation doses is detected by using a Biyuntian CCK8 kit.
Fig. 1 shows that the survival rate of cells gradually decreased with increasing UVB irradiation dose. The UVB radiation dose is preferably over 80% of the cell survival rate, so the UVB dose is selected to be 5mJ/cm2For subsequent experiments.
Example 2
Toxicity of adipic acid on HaCaT cells
HaCaT cells are inoculated in a 96-well plate, when the cells grow to the density of 50%, adipic acid solution (with DMSO as a solvent) with the concentration of 0, 12.5, 25, 50 and 100 mu M is given, and after the cells are cultured for 24 hours, the cell survival rate of the cells under different substance doses is detected by a Biyuntian CCK8 kit.
Fig. 2 shows that adipic acid is not toxic to HaCaT cells over the range of experimental concentrations. Therefore, the maximum nontoxic concentration of 100. mu.M in the experimental range was selected for subsequent experiments.
Example 3
Ameliorating effect on UVB-induced oxidative damage of HaCaT cells
The research is carried out by taking active oxygen (ROS), lipid peroxidation product Malondialdehyde (MDA) and antioxidant enzyme-superoxide dismutase (SOD) as indexes.
1. Reactive Oxygen Species (ROS)
HaCaT cells were seeded in 96-well plates and when grown to 50% density, treated with UVB, UVB + concentration 100 μ M adipic acid, UVB + 0.1% DMSO, respectively, while blank control cells were left untreated (labeled UVB 0); after each group was cultured for 24 hours, the improvement effect of adipic acid on UVB-induced ROS accumulation was detected using a picnic sky ROS detection kit.
HaCaT intracellular ROS levels were characterized by the fluorescence intensity of the DCFH-DA probe. FIG. 3 shows that intracellular ROS levels are very significantly increased after irradiation of HACaT cells with UVB: (****P<0.0001), while post-irradiation intervention with adipic acid can very significantly down-regulate intracellular ROS levels: (****P<0.0001), the solvent DMSO has no effect on the effect of reducing intracellular ROS levels.
2. Lipid peroxidation product Malondialdehyde (MDA)
HaCaT cells were seeded in 6-well plates and when grown to 50% density, treated with UVB, UVB + concentration 100 μ M adipic acid, UVB + 0.1% DMSO, respectively, while blank control cells were left untreated (labeled UVB 0); after each group was cultured for 24 hours, cells were collected and the improvement effect of adipic acid on UVB-induced MDA accumulation was tested using a picnic sky MDA test kit.
FIG. 4 shows that the lipid peroxidation product MDA levels in HaCaT cells are very significantly elevated after the HaCaT cells are subjected to UVB irradiation (***P<0.001) and after irradiation, adipic acid intervention can very significantly reduce intracellular MDA levels (***P<0.001), the solvent DMSO had no effect on the effect of reducing intracellular MDA levels.
3. Antioxidant enzyme-superoxide dismutase (SOD)
HaCaT cells were seeded in 6-well plates and when grown to 50% density, treated with UVB, UVB + concentration 100 μ M adipic acid, UVB + 0.1% DMSO, respectively, while blank control cells were left untreated (labeled UVB 0); after each group was cultured for 24 hours, cells were collected and the effect of improving UVB-induced SOD level reduction by substances was examined using a picnic total SOD assay kit.
FIG. 5 shows that after HaCaT cells were subjected to UVB irradiation, there was a very significant decrease in the level of antioxidant enzyme SOD in HaCaT cells (***P<0.001) and after irradiation, adipic acid intervention can restore very significantly intracellular MDA levels (***P<0.001), the solvent DMSO has no influence on the effect of restoring the intracellular SOD level.
Example 4
Ameliorating effect on UVB-induced oxidative damage of HaCaT cells
1. Influence on the relative expression levels of matrix metalloproteinase 1 gene (MMP-1), matrix metalloproteinase 3 gene (MMP-3), and matrix metalloproteinase 9 gene (MMP-9).
HaCaT cells were seeded in 6-well plates and when grown to 50% density, treated with UVB, UVB + concentration 100 μ M adipic acid, UVB + 0.1% DMSO, respectively, while blank control cells were left untreated (labeled UVB 0); after each group was cultured for another 24 hours, cells were collected.
Real-time PCR analysis: total RNA was extracted with Trizol reagent, and cDNA synthesis was performed according to the reverse transcription kit. Real-time fluorescent quantitative PCR experiments were performed using iQ SYBR green supermix (Bio-Rad). Calculating relative expression levels (CFX Connect) of target genes MMP-1, MMP-3 and MMP-9 by using human beta-actin or GAPDH as internal reference after PCR amplificationTMReal-Time PCR Detection System，Bio-Rad,Hecules,CA,USA)。
FIGS. 6-8 show that after the HaCaT cells are irradiated by UVB, the expression levels of MMP-1 gene, MMP-3 gene and MMP-9 gene in the HaCaT cells are significantly up-regulated ((*P<0.05，****P<0.0001，***P<0.001), and the expression level of MMP-1 and MMP-3 genes can be remarkably reduced by adipic acid intervention after irradiation (*P<0.05，**P<0.01), but the intervention of adipic acid has no obvious influence on the expression level of MMP-9 gene; the solvent DMSO has no influence on the effect of reducing the expression of MMP-1 gene, MMP-3 gene and MMP-9 gene.
2. Influence on the expression level of MMP-1 protein
Cells were seeded in 6-well plates and when grown to 50% density, treated with UVB, UVB + concentration 100 μ M adipic acid, UVB + 0.1% DMSO, respectively, while blank control cells were left untreated (labeled UVB 0); after each group continued to culture for 24 hours, the supernatant and cells were collected.
MMP-1 protein is detected by an elisa kit, and the principle of elisa detection is as follows: fixing MMP-1 detection antibody on the surface of the polystyrene microporous plate by a physical adsorption method, adding a sample to be detected, and indirectly reflecting the content of MMP-1 through the color depth developed by an enzyme label. Finally, MMP-1 protein levels were normalized to the total cellular protein content.
FIG. 9 shows that MMP-1 protein levels secreted by HaCaT cells are extremely significantly increased after the HaCaT cells are subjected to UVB irradiation (****P<0.0001), and the secretion level of MMP-1 protein can be reduced very significantly by adipic acid intervention after irradiation (**P<0.01), the solvent DMSO has no effect on reducing MMP-1 protein secretion levels.
The present invention is not limited to the above-described embodiments, and any variations, modifications, and substitutions which may occur to those skilled in the art may be made without departing from the spirit of the invention.
Claims (10)
1. Use of adipic acid in the manufacture of a product for the treatment of photodamage to skin.
2. Use according to claim 1, wherein the adipic acid is capable of ameliorating UVB-induced oxidative damage of cells.
3. Use according to claim 2, characterized in that the adipic acid is capable of downregulating the expression levels of ROS, MDA and SOD.
4. The use according to claim 2, wherein the adipic acid is capable of down-regulating the relative expression levels of MMP-1, MMP-3 and MMP-9.
5. Use according to claim 2, wherein the adipic acid is capable of down-regulating the expression of MMP-1 protein.
6. A pharmaceutical composition for preventing and/or treating photodamage to skin, comprising adipic acid or a salt thereof according to any one of claims 1 to 5, and a pharmaceutically acceptable adjuvant or carrier.
7. A health food composition for improving skin photoaging, comprising adipic acid or a salt thereof according to any one of claims 1 to 5, and a food-acceptable excipient.
8. The health food composition of claim 7, wherein the health food composition is capable of improving skin wrinkles, enhancing skin elasticity, thinning skin, and reducing pigmentation.
9. Cosmetic composition, characterized in that it comprises adipic acid or a salt thereof according to any one of claims 1 to 5, and at least one cosmetically acceptable adjuvant or carrier.
10. The cosmetic composition as claimed in claim 9, wherein the cosmetic composition is capable of improving skin photoaging and skin aging caused by ultraviolet irradiation.
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Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US5705144A (en) * | 1992-09-30 | 1998-01-06 | Unilever Patent Holdings B.V. | Cosmetic composition containing retinol and dioic acid |
| WO2017142265A1 (en) * | 2016-02-15 | 2017-08-24 | 연세대학교 산학협력단 | Composition containing adipic acid as active ingredient for skin wrinkle alleviation and skin elasticity enhancement |
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2022
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| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US5705144A (en) * | 1992-09-30 | 1998-01-06 | Unilever Patent Holdings B.V. | Cosmetic composition containing retinol and dioic acid |
| WO2017142265A1 (en) * | 2016-02-15 | 2017-08-24 | 연세대학교 산학협력단 | Composition containing adipic acid as active ingredient for skin wrinkle alleviation and skin elasticity enhancement |
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| JIN BOO JEONG等: "Antioxidant activity in essential oils of Cnidium officinale makino and Ligusticum chuanxiong hort and their inhibitory effects on DNA damage and apoptosis induced by ultraviolet B in mammalian cell.", 《CANCER EPIDEMIOLOGY》 * |
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