Active polypeptide OG-RV18 for resisting skin photoaging induced by ultraviolet rays and application of active polypeptide OG-RV18
By developing the peptide OG-RV18 derived from the skin secretions of the giant green frog, the problem of existing technologies being unable to effectively block UVA radiation and repair photoaging damage has been solved, achieving a highly efficient and safe effect in improving skin photoaging.
Patent Information
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2026-01-30
- Publication Date
- 2026-04-03
AI Technical Summary
Existing skin photoaging intervention strategies, such as physical sun protection, antioxidants, and drugs, have limitations. They cannot effectively block UVA radiation, repair photoaging damage, and have irritation or stability issues. There is a lack of highly efficient and safe targeted anti-photoaging molecules.
A polypeptide OG-RV18 derived from the skin secretions of the Yunnan green frog was developed. It has an 18-amino acid sequence RVAAGVGKKLVCGLSGLC and can be used to prepare topical drugs and cosmetics. It can reduce skin wrinkles and improve barrier function by inhibiting UV-induced cell senescence, promoting cell proliferation and migration.
OG-RV18 significantly improves UV-induced photoaging damage to the skin. In vitro and in vivo experiments have shown that it inhibits cell aging, reduces wrinkles, and improves skin barrier function. It is also easy to synthesize, low in cost, and non-toxic, providing a new molecule for anti-photoaging drugs and skin care products.
Smart Images
Figure CN121779508A_ABST
Abstract
Description
Technical Field
[0001] This invention belongs to the field of biomedical technology, specifically relating to an active polypeptide OG-RV18 that resists ultraviolet-induced skin photoaging and its applications. Background Technology
[0002] Photoaging is an accelerated skin aging phenomenon caused by long-term ultraviolet (UVR) radiation, clinically manifested as wrinkles, sagging, pigmentation, and impaired barrier function. Its pathological mechanism lies in the fact that UVA / UVB can induce skin cells to produce reactive oxygen species (ROS), triggering oxidative stress, which in turn activates matrix metalloproteinases (MMPs) to degrade dermal collagen and elastin in large quantities, triggering a persistent inflammatory response, ultimately leading to progressive damage to skin structure and function.
[0003] Currently, clinical intervention strategies for photoaging mainly rely on physical sun protection, antioxidants (such as vitamins C and E), and drugs (such as retinoic acid). However, these methods have significant limitations: physical sun protection only blocks surface UVB, providing insufficient protection against UVA that penetrates the dermis, and cannot repair existing photoaging damage; secondly, small-molecule antioxidants (such as vitamins C and E) can only remove some ROS, but suffer from poor stability and low transdermal efficiency; while drugs such as retinoic acid are effective but highly irritating, easily causing skin erythema, desquamation, and photosensitivity reactions, limiting their long-term use. Therefore, developing novel anti-photoaging molecules that are highly effective, safe, and have good targeting properties has become an urgent need in the field of dermatology.
[0004] Against this backdrop, peptides exhibit unique advantages. Compared to traditional small-molecule drugs, peptides possess characteristics such as high activity, high specificity, and good transdermal absorption. Compared to biologics (such as collagen and epidermal growth factor), peptides have low immunogenicity, making them ideal candidate molecules for skin treatment and care. Amphibians provide valuable resources for discovering such lead molecules; their skin secretes a variety of bioactive peptides to cope with harsh environments (such as strong ultraviolet radiation), forming a natural "treasure trove of functional molecules."
[0005] Based on the above problems, the present invention aims to provide a method for addressing the challenges posed by the Yunnan-native species, the large green stinking frog (Gnaphalium affineum). Odorrana graminea The anti-UV-induced photoaging activity of the skin secretions of this novel peptide is a novel structural peptide. Summary of the Invention
[0006] The first objective of this invention is to provide an active polypeptide OG-RV18 that resists UV-induced skin photoaging, and the second objective of this invention is to provide the application of this polypeptide.
[0007] The first objective of this invention is achieved as follows: the active polypeptide OG-RV18, which is an anti-UV-induced skin photoaging peptide, has the amino acid sequence shown in SEQ ID No. 1: RVAAGVGKKLVCGLSGLC.
[0008] The second objective of this invention is achieved by using the polypeptide OG-RV18 in a topical medicine for treating or improving photoaging of the skin.
[0009] The beneficial effects of this invention are as follows: This invention provides a novel polypeptide, OG-RV18, derived from the Yunnan endemic species, the giant green frog. Experimental verification shows that this polypeptide exhibits significant ameliorative effects on UV-induced photoaging damage of the skin both in vivo and in vitro. Specifically, at the cellular level, OG-RV18 effectively inhibits UVR-induced senescence of HaCat keratinocytes and MSF fibroblasts, while promoting cell proliferation and migration and reducing oxidative stress levels. At the animal level, OG-RV18 significantly reduces skin wrinkle formation, skin roughness, and skin barrier function damage in photoaging model mice. Furthermore, this polypeptide contains only 18 amino acids, is easy to synthesize, low in cost, and non-toxic, providing a new lead molecule for the development of anti-photoaging drugs and a new direction for the development of skincare products that improve photoaging. Attached Figure Description
[0010] Figure 1 This is a primary structure diagram of the polypeptide OG-RV18 of the present invention; Figure 2 The effect of the present invention's polypeptide OG-RV18 on UV-induced senescence of human immortalized keratinocytes (HaCaT) and mouse skin fibroblasts (MSF) (SA-β-Gal staining); wherein, Figure 2 Image A shows HaCaT cells stained with SA-β-Gal. Figure 2 Image B shows MSF cells stained with SA-β-Gal. Figure 2 C represents the quantitative analysis result of the positive rate of SA-β-Gal staining in HaCaT cells; Figure 2 D represents the quantitative analysis result of the positive rate of SA-β-Gal staining in MSF cells; Figure 3 This invention relates to the effects of the polypeptide OG-RV18 on the gross morphology, dermoscopic appearance, and histopathological (H&E staining) of skin in a nude mouse photoaging model. Figure 3 A: From top to bottom, the images show the gross morphology of the skin on the back of a nude mouse, the microscopic appearance of the local skin under a dermoscope, and the histopathological results of the skin tissue after H&E staining. Figure 3 B represents the quantitative statistical results of epidermal thickness of the skin of each group of nude mice. Figure 3C represents the quantitative statistical results of dermal thickness of the skin of each group of nude mice; Figure 4 This invention relates to the effects of the polypeptide OG-RV18 on the physiological functions of skin (elastic recovery time, skin hydration, and transepidermal water loss (TEWL)) in a nude mouse photoaging model. Figure 4 A represents the quantitative statistical results of skin elasticity recovery time. Figure 4 B represents the statistical results of skin moisture content quantification. Figure 4 C represents the quantitative statistical result of transdermal water loss. Detailed Implementation
[0011] The present invention will now be described in further detail with reference to the accompanying drawings and embodiments, but this does not limit the present invention in any way. Any modifications or improvements made based on the teachings of the present invention shall fall within the protection scope of the present invention.
[0012] This invention provides a polypeptide, named OG-RV18, with the amino acid sequence RVAAGVGKKLVCGLSGLC, and its structural formula... Figure 1 As shown. The present invention also provides the use of the polypeptide OG-RV18 in the preparation of topical medicines for treating or improving skin photoaging.
[0013] The topical medication is used to improve one or more related symptoms caused by photoaging: skin laxity and wrinkle formation, pigmentation, epidermal thickening, dermal thinning, collagen loss, or impaired skin barrier function.
[0014] The skin photoaging is induced by ultraviolet radiation.
[0015] The dosage form of the topical medication is a topical cream, gel, or transdermal patch.
[0016] The present invention also provides a pharmaceutical composition comprising a polypeptide OG-RV18 as an active agent and a pharmaceutically acceptable carrier.
[0017] The present invention further provides the application of the polypeptide OG-RV18 in the preparation of cosmetics for anti-photoaging of the skin.
[0018] The present invention further provides a cosmetic composition comprising a polypeptide OG-RV18 and cosmetically acceptable excipients.
[0019] Example 1 Synthesis of peptide OG-RV18 The amino acid sequence of peptide OG-RV18 is RVAAGVGKKLVCGLSGLC, which was developed by Wuhan Baiyixin Biotechnology Co., Ltd. according to the structure of peptide OG-RV18 ( Figure 1Synthesized. The obtained polypeptide had a purity >95% upon testing.
[0020] Example 2: In vitro anti-photoaging activity assay of peptide OG-RV18 Experimental methods: Construction of a cell senescence model and SA-β-Gal staining Human immortalized keratinocytes (HaCaT) and mouse skin fibroblasts (MSF) were used in the experiments. When the cells reached approximately 70% confluence, they were irradiated with a combination of UVA (6 J / cm²) and UVB (30 mJ / cm²) to establish an in vitro skin photoaging model. After irradiation, the cells were randomly divided into three groups: a model group (UVR), a positive control group (UVR + ascorbic acid (Vc), 10 μM), and a peptide treatment group (UVR + OG-RV18, 10 nM). A blank control group was also included. After culturing for another 24 hours, the cells were stained using a β-galactosidase (SA-β-Gal) staining kit, strictly following the manufacturer's instructions. After staining, the cells were observed and photographed under an optical microscope, and the number of blue-positive senescent cells was counted. The SA-β-Gal positive cell rate was statistically analyzed using ImageJ software.
[0021] result: like Figure 2 As shown, compared with the blank control group, the SA-β-Gal positivity rate of HaCaT and MSF cells in the UVR model group was significantly increased. However, compared with the model group, the SA-β-Gal positivity rate in the peptide treatment group (10 nM) was significantly reduced, and its inhibitory effect was close to that of the positive control drug ascorbic acid (10 μM), with a statistically significant difference compared to the model group. This indicates that the peptide OG-RV18 can significantly inhibit UV-induced cell senescence.
[0022] Example 3: In vivo anti-photoaging activity assay of peptide OG-RV18 Experimental Methods: Nude Mouse Skin Photoaging Model Experiment A skin photoaging model was established using 6-8 week old female Balb / c nude mice. The minimum erythema dose (MED) was defined as the combined dose of UVB (60 mJ / cm²) and UVA (6 J / cm²). Animals in the experimental group received UV irradiation every other day for 12 weeks, with the irradiation intensity gradually increasing as follows: 1 MED in weeks 1 and 2, 2 MED in weeks 3 and 4, 3 MED in weeks 5 and 6, and 4 MED from weeks 7 to 12. After successful model establishment, mice were randomly divided into four groups: a model control group (UVR group, UVR + PBS), a positive control group (Vc group, UVR + 10 μM ascorbic acid (Vc)), a low-dose peptide group (UVR + 1 μM OG-RV18), and a high-dose peptide group (UVR + 10 μM OG-RV18). A blank control group (Vehicle group, PBS) was also included. The appropriate drug was applied evenly to the back skin (approximately 4cm × 4cm) of mice every other day, with each application consisting of 50 μL, for a total intervention of 12 weeks. During the intervention, the macroscopic morphology and dermoscopic appearance of the mouse back skin were observed and recorded regularly. After the intervention, back skin tissue was harvested. The skin tissue was fixed, embedded in paraffin, and sectioned for hematoxylin-eosin (H&E) staining. The changes in the tissue structure of the epidermis and dermis were observed using an optical microscope, and the epidermal and dermal thicknesses were quantified using ImageJ software. Using a skin physiological function testing instrument, the transepidermal water loss (TEWL) value, skin hydration, and skin elasticity recovery time of each group of mice were measured after the intervention.
[0023] result: like Figure 3 As shown, treatment with peptide OG-RV18 significantly reduced wrinkle formation on the back of nude mice and improved skin roughness. H&E staining quantification results indicated that peptide OG-RV18 effectively inhibited abnormal epidermal thickening and dermal thinning induced by UVR.
[0024] Skin physiological function test results showed ( Figure 4 Compared with the model control group, mice treated with peptide OG-RV18 showed significantly reduced transepidermal water loss (TEWL), significantly increased skin hydration, and significantly shortened skin elasticity recovery time. Compared with the positive control group, the high-dose group of peptide OG-RV18 (10 μM OG-RV18) showed better improvement in the above three indicators than the positive control drug ascorbic acid (Vc), indicating that peptide OG-RV18 can effectively repair the skin barrier function damaged by UVR.
Claims
1. The polypeptide OG-RV18, with the amino acid sequence RVAAGVGKKLVCGLSGLC, has the structural formula shown in Formula I: I。 2. The use of the polypeptide OG-RV18 of claim 1 in the preparation of a topical medicine for treating or improving skin photoaging.
3. The application according to claim 2, characterized in that, The topical medication is used to improve one or more related symptoms caused by photoaging: skin laxity and wrinkle formation, pigmentation, epidermal thickening, dermal thinning, collagen loss, or impaired skin barrier function.
4. The application according to claim 2, characterized in that, The skin photoaging is induced by ultraviolet radiation.
5. The application according to claim 2, characterized in that, The dosage form of the topical medication is a topical cream, gel, or transdermal patch.
6. A pharmaceutical composition comprising the polypeptide OG-RV18 of claim 1 as an active agent and a pharmaceutically acceptable carrier.
7. The use of the polypeptide OG-RV18 according to claim 1 in the preparation of cosmetics for anti-photoaging of the skin.
8. A cosmetic composition comprising the polypeptide OG-RV18 of claim 1 as an active agent and cosmetically acceptable excipients.