Application of perilla scapes in preparation of cosmetics

Abstract

The invention belongs to the technical field of cosmetics, and particularly relates to application of perilla scapes in preparation of cosmetics with functions of preventing or repairing skin light damage and consolidating skin barrier. According to the application, it is found for the first time that the perilla scapes can effectively avoid skin tissue light damage caused by ultraviolet light, and skin cell sunburn symptoms such as skin erythema, edema, punctiform vascular structure and capillary dilatation, dermatoglyph thickening, epidermis desquamation, cuticle thickening and corium layer diffuse inflammatory cell infiltration caused by the skin tissue light damage are reduced. Meanwhile, the perilla lees can also up-regulate oxidative stress related factors in skin tissues, so that the effect of improving the oxidative injury of the skin is achieved. In addition, the perilla lees can effectively up-regulate the expression level of skin barrier related proteins, and can well participate in differentiation of epidermis cells and formation of skin barriers, so that the perilla lees have the function of consolidating the skin barriers. The perilla lees are used for preparing cosmetics or skin care products for repairing skin light damage, and the perilla lees have wide market application prospects.

Description

TECHNICAL FIELD

[0001] The present application belongs to the technical field of cosmetics, and particularly relates to application of perillartin in preparation of cosmetics for preventing or repairing skin light damage and consolidating skin barrier function. BACKGROUND

[0002] Skin, as the outermost organ of the human body, is extremely vulnerable to environmental damage when exposed to sunlight for a long time. Ultraviolet light is a key factor in causing skin damage from sunlight, which can penetrate the epidermis to reach the epithelial layer of the dermis, causing DNA damage and increasing oxidative stress levels, activating cell signaling pathways, and promoting the expression of specific genes, thereby causing the expression and activation of various intracellular protein kinases, various cytokines, and matrix metalloproteinases, resulting in acute damage (such as sunburn and sunburn) and chronic cumulative damage (such as actinic keratosis, photoaging, and skin cancer) to the skin. Due to the destruction of the ozone layer, the amount of ultraviolet B (UVB) radiation on Earth has increased, which undoubtedly increases the risk of environmental damage to the skin and causes consequences such as photoaging, photoimmunosuppression, and photocarcinogenesis. In addition, as the population ages, the harm of skin light damage to the skin health of the elderly is increasingly prominent, and the incidence of light-related skin tumors is also rising year by year.

[0003] At present, the product used to resist ultraviolet light is mainly a topical sunscreen product. This kind of topical sunscreen product can protect the skin by absorbing or reflecting ultraviolet (UV) radiation on the surface of the skin. Sunscreens are mainly divided into two categories according to their protection mechanism: inorganic compounds and organic compounds. Inorganic compounds belong to inert particles and have the function of reflecting ultraviolet A (UVA) and ultraviolet B (UVB) radiation, and they mainly include zinc oxide and titanium dioxide. These inorganic compounds do not cause skin allergic reactions, but they are visible on the surface of the skin, so from the perspective of aesthetics, inorganic sunscreen is not very popular. Organic sunscreen is usually a carbonyl conjugated aromatic compound, and the conjugated compound can absorb UV and emit lower energy rays to prevent the skin from being damaged by UV radiation. Organic sunscreen is more hidden when applied to the surface of the skin and has better cosmetic properties, but many organic sunscreen ingredients, such as oxybenzone and sulisobenzone, produce photosensitive products when activated by UV, which then interact with the skin, causing adverse skin reactions. For this reason, it is increasingly important to include natural compounds in sunscreen formulations. In the process of oxidative stress-mediated light damage, the endogenous antioxidant capacity of the skin is a key determinant. Most natural compounds have antioxidant effects, and the use of these natural compounds is not only safe, but also can prevent and reduce the occurrence and development of skin diseases caused by ultraviolet radiation.

[0004] Natural compounds are secondary metabolites produced by organisms in nature. Topical application or consumption of natural compounds can prevent skin photodamage. Many natural organic substances can evolve into products with various photorepair mechanisms when exposed to strong radiation, including the production of antioxidants and secondary metabolites that can absorb ultraviolet light.

[0005] Perillartine is a monoterpene component derived from perilla, with a slight perilla aroma. It is a low-calorie, non-toxic high-intensity sweetener with a sweetness of 2000 times that of sucrose. Studies have shown that perillartine can reduce lipid accumulation by inhibiting the transcriptional activity of RORγ, slow down the inflammatory process in the liver, and thus improve glucose and lipid metabolism disorders in the liver. It is a promising compound. So far, there has been no report on the use of perillartine for repairing skin photodamage. SUMMARY

[0006] The present application studies and develops a new application of perillartine. Specifically, it is found that perillartine can be used in the preparation of cosmetics for preventing or repairing skin photodamage and consolidating skin barrier function. The inventors found that ultraviolet radiation can cause skin barrier damage in a mouse skin photodamage model, and perillartine can counteract this damage. As the dose of perillartine increases, the degree of skin damage gradually decreases. Perillartine can also protect the skin from damage caused by ultraviolet radiation by reducing oxidative stress and repairing the skin barrier.

[0007] Therefore, the present application provides the use of perillartine in the preparation of cosmetics for preventing or repairing skin photodamage and consolidating skin barrier function.

[0008] The CAS number of perillartine is 30950-27-7, the molecular formula is C 10 H 15 NO, the molecular weight is 165.23, and the structural formula is: .

[0009] Further, the skin photodamage is skin damage caused by ultraviolet radiation.

[0010] Further, the content of perillartine in the cosmetic is 0.5-2% w / w.

[0011] Further, the perillartine is configured into a perillartine solution for use during use, and the solvent of the perillartine solution is a propylene glycol-95% ethanol mixed solution. The propylene glycol-95% ethanol mixed solution is composed of propylene glycol and ethanol in a weight ratio of 1:1.

[0012] Further, the configuration method of the perillartine solution is: Weigh 1.0 g of perilla stalk, add 100 mL of propylene glycol-95% ethanol mixed solution (w / w=1:1), mix well, and prepare a 2% w / w perilla stalk solution. Take a portion of the solution and dilute it with propylene glycol-95% ethanol mixed solution to 1% w / w and 0.5% w / w for later use.

[0013] Furthermore, the perilla stalk repairs skin photodamage and / or strengthens the skin barrier through any one of (I) to (IV): (I) Reduce epidermal thickness; (II) Increase the content of SOD, CAT, and GSH in the epidermis and decrease the content of MDA; (III) Increase Nrf-2 protein expression; (IV) Increase the expression levels of claudin, occludin and ZO-1 proteins.

[0014] Furthermore, the cosmetics described in this invention are preparations made according to certain dosage form requirements, mainly referring to those that improve skin immunity and strengthen the skin barrier by being applied to the skin surface or acting on the organism through other means. The cosmetics can be gels, facial cleansers, toners, serums, creams, lotions, and moisturizers, but are not limited to these.

[0015] The photodamage to skin tissue in this invention includes symptoms such as skin swelling, purpura, and / or thickening; or telangiectasia, altered vascular structure, patchy distribution of blood vessels forming erythema, increased desquamation, decreased hair growth, coarsened skin texture, and / or disordered skin texture; or significant thickening of the stratum corneum, increased sunburn cells, and / or increased inflammatory cells in the dermis. During their research, the inventors discovered that Perilla frutescens can significantly inhibit symptoms of photodamage to skin tissue such as swelling, purpura, and / or thickening; Perilla frutescens can effectively alleviate symptoms of photodamage to skin tissue such as telangiectasia, altered vascular structure, patchy distribution of blood vessels forming erythema, and reduce symptoms of photodamage to skin tissue such as desquamation, hair loss, coarsened skin texture, and / or disordered skin texture; Perilla frutescens can also significantly reduce the thickness of the stratum corneum, reduce sunburn cells, and / or reduce symptoms of photodamage to skin tissue such as inflammatory cells in the dermis. This invention demonstrates that the perilla lepidium provided by this invention has excellent repair and therapeutic effects on various symptoms of photodamage to skin tissue, and its inhibitory and repair effects are even better with increasing dosage.

[0016] Furthermore, the inventors discovered that perilla stalks can significantly increase the content of SOD, CAT, and GSH in the epidermis and decrease the content of MDA, while increasing the expression level of Nrf-2 protein, thus alleviating oxidative stress. Simultaneously, it can also increase the expression levels of claudin, occludin, and ZO-1 proteins, protecting the skin barrier function. This demonstrates that the perilla stalks provided by this invention have a protective effect on the skin barrier function.

[0017] In addition, the present invention provides a cosmetic with the function of preventing or repairing skin photodamage and strengthening the skin barrier. The cosmetic contains perilla lepidium as a protective agent and excipient for preventing and / or treating skin photodamage. The excipient is at least one of preservatives, chelating agents, fragrances, moisturizers, colorants, emulsifiers, antioxidants and skin conditioning agents.

[0018] In summary, compared with the prior art, the technical solution of the present invention has the following beneficial effects: This invention is the first to discover that perilla lepidium can combat photodamage to skin tissue caused by ultraviolet (UV) light, with the effect becoming more pronounced at higher concentrations. Perilla lepidium can effectively prevent skin erythema, edema, telangiectasia, punctate vascular structures, and increased skin texture caused by UV-induced photodamage. It can also effectively intervene in significant thickening of the stratum corneum and reduce sunburn-related skin cell infiltration. Using this invention, not only can oxidative stress at skin lesions be regulated, increasing the expression of the oxidative stress-related protein Nrf-2 and the content of antioxidant markers SOD, CAT, and GSH in skin tissue, but also reducing the expression of the lipid peroxide MDA, thereby improving the effect of skin oxidative damage; it can also upregulate the expression levels of claudin, occludin, and ZO-1 proteins, which can effectively participate in epidermal cell differentiation and skin barrier formation, thus strengthening the skin barrier function. Therefore, perilla lepidium is a raw material worthy of in-depth research and development for the prevention and treatment of photodamage. Attached Figure Description

[0019] Figure 1 Images of the epidermis on the backs of mice after treatment in each group.

[0020] Figure 2 This is a trend graph showing the percutaneous water loss rate of mice in each group.

[0021] Figure 3 This is a diagram showing the morphological changes of skin lesions in mice.

[0022] Figure 4 This is a bar chart showing the thickness of the epidermis in mouse skin lesions.

[0023] Figure 5 This is a bar chart showing the SOD content at the skin lesions in mice.

[0024] Figure 6 This is a bar chart showing the CAT content at the skin lesions in mice.

[0025] Figure 7 A bar chart showing the GSH content at the skin lesions of mice.

[0026] Figure 8 A bar chart showing the MDA content in mouse skin lesions.

[0027] Figure 9 Figure showing the effect of perilla stalk on the expression of Nrf-2, a protein related to UV oxidative stress in skin.

[0028] Figure 10 A pathological staining image showing the distribution of claudin protein in mouse skin lesions.

[0029] Figure 11 A bar chart showing the claudin content in mouse skin lesions.

[0030] Figure 12 A pathological staining image showing the distribution of occludin protein in mouse skin lesions.

[0031] Figure 13 A bar chart showing the occludin content in mouse skin lesions.

[0032] Figure 14 A pathological staining image showing the distribution of ZO-1 protein in mouse skin lesions.

[0033] Figure 15 A bar chart showing the ZO-1 content in mouse skin lesions. Detailed Implementation

[0034] The present invention will be further described below through specific embodiments, but this is not a limitation of the present invention. Those skilled in the art can make various modifications or improvements based on the basic idea of ​​the present invention, but as long as they do not depart from the basic idea of ​​the present invention, they are all within the scope of the present invention.

[0035] Example 1: Preparation of Perilla Lepidium Solution: Weigh 1.0 g of perilla stalk, add 100 mL of propylene glycol-95% ethanol mixed solution (w / w=1:1), mix well, and prepare a 2% w / w perilla stalk solution. Take a portion of the solution and dilute it with propylene glycol-95% ethanol mixed solution to 1% w / w and 0.5% w / w for later use.

[0036] Example 2: Experimental study on the efficacy of perilla stalk in repairing skin photodamage and strengthening the skin barrier. Experimental methods: 1.1 Animal Model and Group Dosing: Thirty BABL / c mice (Guangdong University of Chinese Medicine, 6-7 weeks old) were randomly divided into five groups of six: a control group, a model group, a high-dose perilla leaf extract group, a medium-dose perilla leaf extract group, and a low-dose perilla leaf extract group. Hair was removed from the backs of all mice in each group, creating an area approximately 2 cm × 4 cm in size. The control group received only petroleum jelly applied to their backs daily. All other groups received 200 mJ / cm² perilla leaf extract daily. 2 To induce photodamage in the skin and establish a photodamage model, mice were euthanized 4 hours after modeling each day, except for the control group. Each mouse received 0.2 mL of the corresponding drug solution once daily. Dosage was as follows: The perilla leaf solution prepared in Example 1 was used. Perilla leaf was administered at regular intervals daily at high doses (200 mg / kg·d), medium doses (100 mg / kg·d), and low doses (50 mg / kg·d). The model group received an equal volume of propylene glycol-95% ethanol mixture. After 28 days of continuous administration, mice were euthanized by cervical dislocation under anesthesia on day 29. Tissue samples from the corresponding skin lesions in each group were harvested and fixed in 4% paraformaldehyde solution.

[0037] 1.2 Detection Indicators and Methods: 1.2.1 Observation of skin changes and measurement of transdermal water loss (TEWL) in mice: The morphological changes of skin lesions in each group of mice were recorded using digital photography. During the pretreatment stage, the hairless areas on the backs of the mice were cleaned with 75% ethanol solution. Barrier function was then assessed using a calibrated Tewameter®™ 300 probe (Courage+Khazaka electronic GmbH, Germany). During measurement, the probe pressure was fixed at 4.9 N / cm², and dynamic data were continuously collected for 20 seconds at a uniform anatomical site. This duration was determined based on the principle of optimal instrument signal-to-noise ratio and preliminary experimental results. Each measurement site was measured three times, with a 60-second interval between adjacent measurements to eliminate the influence of local microenvironment disturbances. The arithmetic mean was taken as the observed value at that time point.

[0038] 1.2.2. Morphology of mouse skin lesions: Hematoxylin-eosin (HE) staining and Masson staining were used, respectively. Tissue from lesions fixed in 4% paraformaldehyde solution was dehydrated, embedded, sectioned, and stained. Epidermal thickness was measured using Image-Pro Plus 6.0 image analysis software after photographing under a 200x objective lens.

[0039] 1.2.3. Pathological examination of mouse skin lesions: Immunohistochemistry was used to detect the expression of claudin, occludin, and ZO-1 proteins in mouse skin lesions. Paraffin sections from section 1.2.2 were dewaxed, subjected to gradient ethanol treatment, and blocked. Primary antibodies against claudin, occludin, and ZO-1 rabbit monoclonal antibodies were added, and the sections were incubated at room temperature for 1 h. Goat anti-rabbit HPR secondary antibody was then added, and the sections were incubated at room temperature for 1 h. Freshly prepared DAB chromogenic solution was added for development, followed by hematoxylin counterstaining for approximately 3 min. After dehydration and mounting, the sections were photographed under a white light microscope. The expression of these proteins was analyzed using Image-Pro Plus 6.0 image analysis software, and the results are expressed as average optical density (IOD).

[0040] 1.2.4. Determination of SOD, MDA, GSH, and CAT activity in mouse dorsal skin tissue: Remove mouse back tissue from a -80 ℃ freezer and accurately weigh 50 mg of tissue. Mince the tissue and add RIPA lysis buffer containing 1% PMSF at a mass (mg):volume (μL) ratio of 1:20. Homogenize the tissue under ice-water bath conditions and centrifuge at 12000 rpm for 10 min. Collect the supernatant for later use. For the determination of SOD, MDA, CAT, and GSH, refer to the kit instructions.

[0041] 1.2.5. Western blot analysis of the effects on related proteins: Samples were collected while observing changes in mouse skin, and Western blot was used to detect the effect of each treatment on the expression of Nrf-2, a protein related to oxidative stress, in a mouse skin photodamage model.

[0042] (1) Protein denaturation treatment: Total protein was extracted from mouse dorsal skin tissue and BCA quantification was performed. An equal amount of protein sample (30 μg) was mixed with 5×SDS-PAGE loading buffer at a volume ratio of 4:1, heat-denatured in a metal bath at 95 ℃ for 5 min, centrifuged at 12000×g for 1 min, and immediately placed on ice for later use.

[0043] (2) Gradient gel preparation: The Bio-Rad Mini-PROTEAN Tetra system was used to test the seal by assembling a 1.5 mm thick glass plate and injecting it with ultrapure water. An 8% separating gel (acrylamide / Bis 29:1, pH 8.8 Tris-HCl, 0.1% SDS, 0.05% APS, 0.1% TEMED) was prepared and polymerized for 30 min. After removing the surface water layer, a 5% stacking gel (acrylamide / Bis 29:1, pH 6.8 Tris-HCl, 0.1% SDS, 0.05% APS, 0.1% TEMED) was poured in and inserted into a 10-well comb for static polymerization.

[0044] (3) Electrophoretic separation: Add the denatured sample to the gel wells and perform vertical electrophoresis with pre-cooled Tris-Glycine-SDS electrophoresis buffer (25 mM Tris, 192 mM Glycine, 0.1% SDS). During the concentration phase, electrophoresis is performed at a constant voltage of 80 V until the bromophenol blue migrates to the separating gel interface. Then, the voltage is adjusted to 120 V and electrophoresis is stopped when the indicator migrates to 0.5 cm from the bottom of the gel.

[0045] (4) Wet electrotransfer printing: Gels within the target molecular weight range were cut, and PVDF membranes were activated with methanol and assembled with the gel, filter paper, and sponge pads to form a "sandwich" structure. The membranes were then transferred at a constant current of 300 mA for 90 min at 4 °C in pre-cooled transfer buffer (25 mM Tris, 192 mM Glycine, 20% methanol).

[0046] (5) Membrane sealing: Immediately after transfer, the PVDF membrane was immersed in 5% BSA / TBST blocking solution (20 mM Tris-HCl, 150 mM NaCl, 0.1% Tween-20, pH 7.6) and blocked at room temperature on a horizontal shaker (60 rpm) for 2 h.

[0047] (6) Immune response: Primary antibody incubation: After blocking, the membrane was incubated with Nrf-2 (1:1000), Smad2 / 3 (1:2000), and ERK / P-ERK (1:1500) specific primary antibodies at 4 °C with shaking for 16 h; Washing: TBST was used for room temperature shaking and washing (5 × 5 min, 100 rpm); Secondary antibody incubation: HRP-labeled goat anti-rabbit IgG (1:5000) was used for room temperature shaking and incubation for 1 h, followed by washing and use.

[0048] (7) Chemiluminescence detection of ECL: The substrate working solution (solution A:solution B = 1:1, v / v) was uniformly applied to the membrane surface under light-protected conditions, and chemiluminescence signals were acquired using the ChemiDoc MP imaging system. β-actin (1:3000) was used as an internal control for standardization, and band grayscale analysis was performed using Image-Pro Plus 6.0 software. Data for each group are expressed as the ratio of the target protein to the internal control.

[0049] 1.3 Statistical methods: Statistical analysis of experimental data uses the mean and standard deviation (SD) as the basis for calculation. The data were analyzed using GraphPad Prism 10.1.2 software. Homogeneity of variance was determined using one-way ANOVA, and unequal variances were analyzed using nonparametric tests. P <0.05 indicates statistical significance.

[0050] 2. Experimental Results: 2.1 The effects of Perilla frutescens on a mouse model of photodamage to the skin are as follows: Figure 1 and Figure 2 As shown.

[0051] Figure 1 Images of the epidermis on the backs of mice after treatment in each group. Figure 2 Trend graph of transdermal water loss rate in each group of mice ( (n=6).

[0052] Depend on Figure 1 and Figure 2 The results showed that the control group mice had smooth and even skin, while the model group mice exhibited significant skin damage characteristics after UVB radiation, including localized epidermal thickening, large-area crusting, and erythema-like lesions, as well as photodamage phenotypes such as decreased elasticity and wrinkle formation. Compared with the model group, the skin erythema was reduced and the skin was smoother and more even with less infiltration in each dose group of Perilla frutescens, indicating that Perilla frutescens can significantly improve the UVB-induced photodamage-like phenotype. Furthermore, the TEWL (transmissible wound healing) in each dose group of Perilla frutescens was lower than that in the model group at the same time point. These results, combined with the above findings, suggest that Perilla frutescens can protect the skin barrier function from photodamage.

[0053] 2.2 The effects of Perilla frutescens on the histological changes of skin lesions in a mouse model of psoriasis are as follows: Figure 3 and Figure 4 As shown.

[0054] Figure 3 Morphological changes of skin lesions in mice (HE, 200×). Figure 4 A bar chart showing the thickness of the epidermis in mouse skin lesions ( (n=6). Compared with the blank group, #### P<0.0001; compared with the model group, * P <0.05, ** P <0.005.

[0055] Depend on Figure 3 and Figure 4 It was found that in HE-stained skin tissue sections of mice, the stratum corneum of the blank group was intact and of uniform thickness. The cells of the granular layer and spinous layer were neatly arranged and regularly shaped. The nuclei of the basal layer cells were oval and the nuclear-cytoplasmic ratio was stable. No vacuolar degeneration or nuclear pyknosis was observed. The epidermis of the model group was significantly thickened, with alternating areas of hyperkeratosis and parakeratosis, and localized sheet-like shedding of the stratum corneum was visible. The polarity of the spinous cell layer cells was disordered, and scattered apoptotic bodies were visible. Vasoblastic degeneration and nuclear dissolution were observed in the basal layer. The dermis showed vasodilation with infiltration of polymorphonuclear leukocytes. Hair follicles entered the regression phase, and the number of sebaceous gland acini decreased. Compared with the model group mice, the epidermis of mice in each dose group of Perilla frutescens was smoother, the number of parakeratotic cells was significantly reduced, the dermis was thinner, and the thickness of the epidermis was significantly lower than that of the model group, with statistically significant differences. P <0.01), among which the epidermal layer thickness decreased most significantly in the high-dose group of perilla lepidium.

[0056] 2.3. The effect of perilla stalk on oxidative stress in the skin of photodamaged mice is as follows: Figures 5-9 As shown.

[0057] 2.3.1 Biochemical results of perilla leaf on oxidative stress in photo-damaged mouse skin are as follows: Figures 5-8 As shown: Figure 5 A bar chart showing the SOD content at mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001. Figure 6 A bar chart showing the CAT content at mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001. Figure 7 A bar chart showing the GSH content at mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001. Figure 8 A bar chart showing the MDA content at mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001.

[0058] Depend on Figure 5 , Figure 6 , Figure 7 and Figure 8 It can be seen that, compared with the blank group, the levels of SOD, CAT, and GSH in the epidermis of the model group were significantly reduced, while the level of MDA was significantly increased, which was statistically significant. P <0.01). Compared with the model group, all doses of Perilla frutescens showed an increase in the content of SOD, CAT, and GSH in the epidermis and a decrease in the content of MDA, indicating that Perilla frutescens can significantly increase the content of SOD, CAT, and GSH in the epidermis and decrease the content of MDA, thus alleviating oxidative stress.

[0059] 2.3.2. Western Blot results of the effect of perilla stalk on oxidative stress in the skin of photodamaged mice are as follows: Figure 9 As shown: Figure 9 Figure showing the effect of perilla stalk on the expression of Nrf-2, a protein related to UV oxidative stress in skin. (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001.

[0060] Depend on Figure 9 It was found that, compared with the control group, the Nrf-2 protein content in the epidermis of the model group was significantly reduced. However, after treatment with perilla stalk, the expression of the oxidative stress-related protein Nrf-2 significantly increased, showing a dose-response effect.

[0061] 2.4. The effects of Perilla frutescens on skin barrier-related proteins in photodamaged mice are as follows: Figures 10-15 As shown.

[0062] Figure 10 A pathological staining image of claudin protein distribution in mouse skin lesions (IHC, 200×). Figure 11 A bar chart showing the claudin content in mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001. Figure 12Pathological staining image of occludin protein distribution in mouse skin lesions (IHC, 200×). Figure 13 A bar chart showing the occludin content in mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001. Figure 14 Pathological staining image of ZO-1 protein distribution in mouse skin lesions (IHC, 200×). Figure 15 A bar chart showing the ZO-1 content in mouse skin lesions ( (n=6); compared with the blank group, #### P <0.0001; compared with the model group, **** P <0.0001.

[0063] Depend on Figures 10-15 It was found that, in the immunohistochemical results of Claudin and occludin proteins, compared with the blank group, the levels of claudin, occludin, and ZO-1 in the epidermis of the model group were significantly reduced, which was statistically significant. P <0.01). Compared with the model group, high doses of Perilla frutescens all showed a promoting effect on the expression of claudin, occludin, and ZO-1 proteins in the epidermis. In conclusion, Perilla frutescens has a protective effect on skin barrier function.

[0064] 3. Experimental conclusions: This invention uses naturally sourced perilla lepidium to prepare cosmetics for improving skin immunity and strengthening the skin barrier. The technology of this invention can combat photodamage to skin tissue caused by ultraviolet (UV) radiation, with higher concentrations showing more pronounced effects. The perilla lepidium provided by this invention can effectively prevent photodamage to skin tissue caused by UV radiation, reducing skin erythema, edema, punctate vascular structures and telangiectasia, thickened skin lines, and excessive desquamation. Simultaneously, it can effectively intervene in stratum corneum thickening and reduce skin cell sunburn phenomena such as diffuse inflammatory cell infiltration in the dermis. This perilla lepidium can also upregulate the expression of the oxidative stress-related protein Nrf-2, upregulate the content of oxidative stress-related factors SOD, CAT, and GSH in skin tissue, and inhibit the expression of lipid peroxide MDA, thereby achieving the effect of improving skin oxidative damage. In addition, this perilla stalk can effectively upregulate the expression levels of claudin, occludin and ZO-1 proteins, and can participate well in the differentiation of epidermal cells and the formation of the skin barrier, thus having the function of strengthening the skin barrier. It can be used to prepare cosmetics or skin care products that repair photodamage to the skin.

[0065] The above embodiments are preferred embodiments of the present invention, but the embodiments of the present invention are not limited to the above embodiments. Any changes, modifications, substitutions, combinations, or simplifications made without departing from the spirit and principle of the present invention shall be considered equivalent substitutions and shall be included within the protection scope of the present invention.

Claims

1. Application of perilla stalk in the preparation of cosmetics that prevent or repair skin photodamage and strengthen the skin barrier.

2. The application as described in claim 1, characterized in that, The aforementioned photodamage to the skin is skin damage caused by ultraviolet radiation.

3. The application as described in claim 1, characterized in that, The content of perilla stalk in cosmetics is 0.5-2% w / w.

4. The application as described in claim 1, characterized in that, The perilla lepidium repairs skin photodamage and / or strengthens the skin barrier through any of (I) to (IV): (I) Reduce epidermal thickness; (II) Increase the content of SOD, CAT, and GSH in the epidermis and reduce the content of MDA; (III) Increase Nrf-2 protein expression; (IV) Increase the expression levels of claudin, occludin, and ZO-1 proteins.

5. The application as described in claim 1, characterized in that, The cosmetics include gels, facial cleansers, toners, serums, creams, lotions, and moisturizers.

6. A cosmetic product that prevents or repairs skin photodamage and strengthens the skin barrier, characterized in that, It contains perilla stigma as a protective agent and excipient for the prevention and / or treatment of photodamage to the skin.

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