Application of bulbus lilii glycoside B
Wanglihe glycoside B, as an active ingredient in products for skin photoaging, solves the stability and permeability problems of existing ingredients by improving cell vitality and collagen gene expression, and significantly improves UVA-induced skin photoaging.
Patent Information
- Application Number
- CN202511377761.3
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-09-25
- Publication Date
- 2025-10-31
AI Technical Summary
Existing anti-photoaging ingredients such as vitamin C, vitamin E and coenzyme Q10 have limitations in terms of stability, permeability and bioavailability, making it difficult to effectively prevent and treat UVA-induced photoaging diseases.
Using lily glycoside B as the active ingredient, products for the prevention or treatment of photoaging skin diseases, including cosmetics and pharmaceuticals, are prepared. By improving cell vitality, reducing the number of β-galactosidase positive cells, reducing lipofuscin deposition, and increasing collagen gene expression levels, UVA-induced photoaging of the skin is improved.
It significantly improves cell vitality, reduces aging markers in skin fibroblasts, and improves skin photoaging, especially showing important therapeutic effects on UVA-induced skin photoaging.
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Figure CN120860041A_ABST
Abstract
Description
Technical Field
[0001] This invention relates to the application of lily glycoside B in the preparation of products for the prevention and / or treatment of photoaging skin diseases, and belongs to the field of photoaging prevention and treatment technology. Background Technology
[0002] Ultraviolet (UV) radiation is light from sunlight with wavelengths of 100–400 nanometers (nm). It can be divided into three types: UVA (ultraviolet A, wavelength 320–400 nm, long-wave), UVB (wavelength 280–320 nm, medium-wave), and UVC (wavelength 100–280 nm, short-wave). UVA has extremely strong penetrating power, reaching deep into the dermis and damaging collagen and elastin fibers, leading to photoaging phenomena such as loss of skin elasticity, wrinkles, sagging, and roughness. Furthermore, UVA is present year-round and can penetrate even on cloudy days and indoors (through glass). The damage accumulated over time is often difficult to detect, and by the time it is noticed, significant damage has already occurred. Studies have shown that UVA's sunburn and redness-inducing effects are 1000 times greater than UVB's, and long-term accumulation leads to photoaging and severe skin damage.
[0003] Currently, anti-photoaging strategies mainly focus on anti-oxidation, anti-inflammation, and promoting collagen synthesis. Common anti-photoaging ingredients include vitamin C, vitamin E, coenzyme Q10, and green tea extract ([J]. Journal of the American Academy of Dermatology, 2012, 67(5)). These ingredients delay skin aging by scavenging free radicals, inhibiting the release of inflammatory factors, or promoting collagen production. However, these ingredients have certain limitations in practical applications. For example, although vitamin C has a strong antioxidant effect, its stability is poor and it is easily oxidized and inactivated; vitamin E has limited permeability and is difficult to effectively reach the deep layers of the skin; coenzyme Q10 has low bioavailability and limited effect. Therefore, developing new, efficient, stable, and safe anti-photoaging ingredients has become a current research hotspot.
[0004] Regaloside B (CAS No. 114420-67-6) is a natural active ingredient extracted from plants of the Liliaceae family, and has the chemical structural formula shown in Formula I:
[0005] .
[0006] Although existing studies have shown that lily glycoside B has antioxidant and anti-inflammatory effects ([J]. Journal of Ethnopharmacology, 2021, 270:113852) and ([J]. Journal of Analytical Testing, 2018, 37(9)), there are still no reports on the use of lily glycoside B in the prevention and / or treatment of photoaging diseases of the skin, especially no reports on the application of lily glycoside B in preventing and treating photoaging diseases of the skin caused by UVA. Summary of the Invention
[0007] The purpose of this invention is to provide the application of lily glycoside B in the preparation of products for the prevention and / or treatment of photoaging skin diseases, thus providing a new approach to the treatment of photoaging skin diseases.
[0008] The application described in this invention refers to the use of lily glycoside B as the sole active ingredient or one of the active ingredients in the preparation of products for the prevention and / or treatment of photoaging skin diseases.
[0009] Furthermore, the photoaging is UVA-induced photoaging.
[0010] Furthermore, the aforementioned photoaging skin diseases include, but are not limited to: actinic keratosis, squamous cell carcinoma, malignant melanoma, etc.
[0011] Furthermore, the product in question is a cosmetic or a pharmaceutical.
[0012] Furthermore, the cosmetics mentioned are skincare products or cosmetics containing skincare functions.
[0013] Furthermore, the dosage form of the cosmetic includes at least one of the following: liquid, emulsion, cream, ointment, gel, patch, and spray.
[0014] Furthermore, the drug also includes pharmaceutically acceptable excipients.
[0015] Furthermore, the pharmaceutically acceptable excipients include at least one of the following: diluents, binders, wetting agents, lubricants, disintegrants, solvents, emulsifiers, cosolvents, solubilizers, preservatives, pH adjusters, osmotic pressure adjusters, surfactants, coating materials, antioxidants, antibacterial agents, and buffers.
[0016] Furthermore, the dosage form of the medicine includes at least one of granules, capsules, powders, tablets, pills, emulsions, suspensions, syrups, ointments, injections, suppositories, aerosols, gels, patches, and drops.
[0017] Furthermore, the route of administration of the drug includes at least one of sublingual administration, oral administration, transdermal administration, injection administration, and spray administration.
[0018] Compared with the prior art, the present invention has the following significant advantages:
[0019] The experimental results of this invention show that: Wangbaihe glycoside B can significantly improve the cell viability of UVA-induced human skin fibroblasts, reduce the number of β-galactosidase-positive cells and decrease lipofuscin deposition in UVA-induced human skin fibroblasts, significantly improve UVA-induced photoaging of skin fibroblasts, significantly improve the photoaging grade of the skin on the back of C57BL / 6 mice induced by UVA, and increase the relative mRNA expression levels of type I collagen gene COL1A1 and type III collagen gene COL3A1; therefore, Wangbaihe glycoside B is expected to be used as an active ingredient in pharmaceuticals or cosmetics for the prevention and / or treatment of skin photoaging diseases, especially for the prevention and / or treatment of UVA-induced skin photoaging diseases, which has important significance and significant application value. Attached Figure Description
[0020] Figure 1 The figure shows the cell viability of skin fibroblasts in each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ## indicates comparison with the model control group, p < 0.01; ### indicates comparison with the model control group, p < 0.001.
[0021] Figure 2a These are photographs of β-galactosidase staining in skin fibroblasts from each experimental group;
[0022] Figure 2b The percentage of β-galactosidase-positive cells in skin fibroblasts in each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ### indicates comparison with the model control group, p < 0.001;
[0023] Figure 3a These are photographs of lipofuscin staining in skin fibroblasts from each experimental group;
[0024] Figure 3b The figure shows the level of lipofuscin deposition in skin fibroblasts in each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ### indicates comparison with the model control group, p < 0.001.
[0025] Figure 4a The figures show the relative mRNA expression levels of the p21 gene in skin fibroblasts of each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ## indicates comparison with the model control group, p < 0.01.
[0026] Figure 4bThe figures show the relative mRNA expression levels of the p53 gene in skin fibroblasts of each experimental group; in the figure: ** indicates comparison with the blank control group, p < 0.01; # indicates comparison with the model control group, p < 0.05;
[0027] Figure 4c The figures show the relative mRNA expression levels of the MMP1 gene in skin fibroblasts of each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ## indicates comparison with the model control group, p < 0.01; ### indicates comparison with the model control group, p < 0.001.
[0028] Figure 4d The figures show the relative mRNA expression levels of the MMP9 gene in skin fibroblasts of each experimental group. In the figure: *** indicates a comparison with the blank control group, p < 0.001; # indicates a comparison with the model control group, p < 0.05; ## indicates a comparison with the model control group, p < 0.01; ### indicates a comparison with the model control group, p < 0.001.
[0029] Figure 4e The figures show the relative mRNA expression levels of the COL1A1 gene in skin fibroblasts of each experimental group. In the figure: *** indicates a comparison with the blank control group, p < 0.001; # indicates a comparison with the model control group, p < 0.05; ## indicates a comparison with the model control group, p < 0.01.
[0030] Figure 4f The figures show the relative mRNA expression levels of the COL3A1 gene in skin fibroblasts of each experimental group; in the figure: *** indicates comparison with the blank control group, p < 0.001; ### indicates comparison with the model control group, p < 0.001.
[0031] Figure 5 The figures show the effects of each experimental group on the grading of UVA-induced photoaging of the dorsal skin of C57BL / 6 mice; in the figure: *** indicates comparison with the blank control group, p < 0.001; ### indicates comparison with the model control group, p < 0.001.
[0032] Figure 6a The figure shows the relative expression level of COL1A1 gene mRNA in the dorsal skin of C57BL / 6 mice; in the figure: *** indicates comparison with the blank control group, p < 0.001; ## indicates comparison with the model control group, p < 0.01.
[0033] Figure 6bThe figure shows the relative expression level of the COL3A1 gene mRNA in the dorsal skin of C57BL / 6 mice; in the figure: *** indicates comparison with the blank control group, p < 0.001; ## indicates comparison with the model control group, p < 0.01. Detailed Implementation
[0034] The present invention will be further illustrated below with reference to specific embodiments. It should be understood that these embodiments are for illustrative purposes only and are not intended to limit the scope of the invention. Experimental methods in the following embodiments, unless otherwise specified, are generally performed under conventional conditions or as recommended by the manufacturer. Unless otherwise specified, the materials, reagents, etc., used in the following embodiments are commercially available. The compound Wangbaihe glycoside B used in the following embodiments was purchased from Shanghai Shidande Standard Technical Service Co., Ltd., and its purity is higher than 95%.
[0035] Example 1: Investigating the effect of lily glycoside B on UVA-induced cell viability of skin fibroblasts
[0036] (1) HFF-1 cell culture
[0037] Remove the cryovials containing HFF-1 cells from the liquid nitrogen container and quickly place them in a 37°C water bath, shaking continuously, to thaw them completely within 1 minute. Add the thawed cell suspension to a centrifuge tube containing 5 mL of DMEM medium and incubate at 1000 rpm at room temperature. -1 Centrifuge for 5 min, then discard the supernatant, add 1 mL of high-glucose DMEM medium to resuspend, transfer to a large dish, add DMEM medium containing 15% FBS, mix well, and culture at 37℃ and 5% CO2 until the cells adhere. Then change the medium and continue culturing. When the cells reach 80% confluence, passage them. All experimental cells are kept within 8 to 15 passages.
[0038] (2) Paving
[0039] Count HFF-1 cells at 5 × 10⁻⁶. 3 Cells were seeded at a density of / well in DMEM 96-well plates containing 15% FBS and divided into blank control group, model control group and drug administration groups with different concentrations. All cells were cultured overnight at 37°C in a 5% CO2 incubator.
[0040] (3) Administration
[0041] After the cells adhered to the cell wall, Wangbaihe glycoside B was added to the drug treatment groups at final concentrations of 25, 50, and 100 μM, respectively, and the cells were stabilized in a cell culture incubator for 1 h.
[0042] (4) Modeling
[0043] The model control group and the drug-treated group were irradiated with UVA at 300 mJ / cm².2 Irradiate for 40 minutes each day for 3 consecutive days.
[0044] (5) Determine cell viability
[0045] On day 4, 100 μL of 10% CCK-8 reagent was added to each well of each experimental group. A blank control group was also set up (no drug administration or modeling, only DMEM containing 15% FBS was added). After incubating each experimental group at 37°C for 1 hour, the absorbance of each well was measured at 490 nm using a microplate reader, and cell viability was calculated using the following formula:
[0046] Cell Viability = [(As - Ab) / (Ac - Ab)] × 100%, where As is the absorbance value of the experimental group, Ab is the absorbance value of the blank control group, and Ac is the absorbance value of the model control group.
[0047] Please see Table 1 and Table 2 for detailed experimental results. Figure 1 As shown.
[0048] Table 1. Cell viability of skin fibroblasts in each experimental group
[0049]
[0050] Note: Graphing and data analysis were performed using Prism software. A p < 0.05 was considered statistically significant. *** indicates a comparison with the blank control group, p < 0.001; ## indicates a comparison with the model control group, p < 0.01; ### indicates a comparison with the model control group, p < 0.001.
[0051] Combining Table 1 and Figure 1 The results show that lily glycoside B can significantly improve the cell viability of skin fibroblasts induced by UVA.
[0052] Example 2: Investigating the effect of lily glycoside B on UVA-induced senescence markers in skin fibroblasts
[0053] (1) HFF-1 cell culture
[0054] Same as described in Example 1.
[0055] (2) Paving
[0056] HFF-1 cells were loaded at 5 × 10 3 Cells were seeded at a density of / well in DMEM 6-well plates containing 15% FBS and divided into blank control group, model control group and drug administration groups with different concentrations. All cells were cultured overnight at 37°C in a 5% CO2 incubator.
[0057] (3) Administration
[0058] Same as described in Example 1.
[0059] (4) Modeling
[0060] Same as described in Example 1.
[0061] (5) β-galactosidase staining
[0062] A blank control group (no drug administration or modeling, only DMEM containing 15% FBS) was set up. Cell culture medium was aspirated from the 6-well plates, and cells were washed once with PBS. 1 mL of β-galactosidase staining and fixation solution was added, and the cells were fixed at room temperature for 15 min. The cell fixation solution was then aspirated, and the cells were washed three times with PBS for 3 min each time. PBS was then aspirated, and 1 mL of staining working solution was added to each well. The cells were incubated overnight at 37°C. Finally, the cells were observed and counted under a light microscope. Detailed experimental results are shown in Table 2 and [Table data missing]. Figure 2a and Figure 2b As shown.
[0063] (6) Lipofuscin staining
[0064] A blank control group was set up (no drug administration or modeling, only DMEM containing 15% FBS was added). Cell culture medium was aspirated from the 6-well plates, washed once with distilled water, air-dried, and then fixed with SBB fixative for 15 min. The fixative was removed by washing with distilled water for 10 seconds, and the plates were slightly air-dried. Freshly prepared SBB staining working solution was added, and the plates were stained at room temperature for 60 min. Excess stain was then washed away with 70% ethanol, followed by rinsing with distilled water for 1 min, staining with Wright's stain for 30 min, and then quickly washed away with distilled water to remove excess stain. Finally, the plates were air-dried and examined under a microscope. Detailed experimental results are shown in Table 3 and [Table data missing]. Figure 3a and Figure 3b As shown.
[0065] Table 2. Percentage of β-galactosidase-positive cells in skin fibroblasts of each experimental group
[0066]
[0067] Note: Graphing and data analysis were performed using Prism software. A p < 0.05 was considered statistically significant between groups; *** indicates a comparison with the blank control group, p < 0.001; ### indicates a comparison with the model control group, p < 0.001.
[0068] Table 3. Relative levels of lipofuscin deposition in skin fibroblasts of each experimental group
[0069]
[0070] Note: Graphing and data analysis were performed using Prism software. A p < 0.05 was considered statistically significant between groups; *** indicates a comparison with the blank control group, p < 0.001; ### indicates a comparison with the model control group, p < 0.001.
[0071] Combine Table 2 and Figure 2a and Figure 2b The results show that: the blank control group had fewer β-galactosidase positive cells; compared with the blank control group, the number of β-galactosidase positive cells in the model control group was significantly increased; and compared with the model control group, administration of Wangbaihe glycoside B significantly reduced the number of β-galactosidase positive cells in a dose-dependent manner.
[0072] Combined with Table 3 and Figure 3a and Figure 3b The results show that: there was almost no lipofuscin deposition in the blank control group; compared with the blank control group, the lipofuscin deposition in the model control group was significantly increased; and compared with the model control group, administration of lily glycoside B significantly reduced the deposition of lipofuscin in HFF-1 cells in a dose-dependent manner.
[0073] Example 3: Investigating the relative expression levels of senescence-related genes (p21, p53), matrix metalloproteinases (MMP-1, MMP-9), and type I collagen (COL1A1) and type III collagen (COL3A1) mRNA in UVA-induced photoaged human skin fibroblasts.
[0074] (1) HFF-1 cell culture
[0075] Same as described in Example 1.
[0076] (2) Paving
[0077] Same as described in Example 2.
[0078] (3) Administration
[0079] Same as described in Example 1.
[0080] (4) Modeling
[0081] Same as described in Example 1.
[0082] (5) Real-time quantitative PCR
[0083] A blank control group (no drug administration or modeling, only DMEM containing 15% FBS) was set up. Cell culture medium was aspirated from the 6-well plates, and the cells were washed three times with PBS. 1 mL of Trizol reagent was added to each well for lysis. 1 / 5 volume of chloroform was added, the mixture was vigorously vortexed, and the plates were allowed to stand at room temperature. The mixture was centrifuged, the supernatant was transferred, and an equal volume of pre-chilled isopropanol was added. The plates were allowed to stand at room temperature, centrifuged, and the supernatant was discarded. The RNA precipitate was washed with pre-chilled 75% ethanol, air-dried at room temperature, and then dissolved in an appropriate volume of DEPC water. The concentration of the extracted RNA was quantified, and then reverse transcription was performed to obtain cDNA. This cDNA was used as a template for subsequent amplification. The amplification system was prepared as follows: 0.5 μL cDNA, 2 μL primer mixture (containing upstream and downstream primers), 5 μL 2×ChamQ Universal SYBR qPCR Master Mix, and 2.5 μL ddH2O. Primer sequences are shown in Table 4.
[0084] Table 4 Primer Sequences
[0085]
[0086] Please see Table 5 for detailed experimental results. Figures 4a-4f As shown.
[0087] Table 5. Relative mRNA expression levels of aging-related genes in fibroblasts of each experimental component.
[0088]
[0089] Note: Prism software was used for graphing and data analysis. A p < 0.05 was considered statistically significant between groups; ** indicates a comparison with the blank control group, p < 0.01; *** indicates a comparison with the blank control group, p < 0.001; # indicates a comparison with the model control group, p < 0.05; ## indicates a comparison with the model control group, p < 0.01; ### indicates a comparison with the model control group, p < 0.001.
[0090] Combined with Table 5 and Figures 4a-4f The results show that: Wanglihe glycoside B can significantly reduce the relative mRNA expression levels of aging-related genes (p21, p53) and matrix metalloproteinase genes (MMP1, MMP9) in skin fibroblasts induced by UVA, and can significantly increase the relative mRNA expression levels of type I collagen gene COL1A1 and type III collagen gene COL3A1.
[0091] Example 4: Investigating the effect of lily glycoside B on UVA-induced photoaging grading of dorsal skin in C57BL / 6 mice
[0092] C57BL / 6 mice were purchased from the Animal Experiment Center of Shanghai University of Traditional Chinese Medicine and then housed at Beijing Vital River Laboratory Animal Technology Co., Ltd. The mice were kept in the laboratory of the Animal Experiment Center of Shanghai University of Traditional Chinese Medicine under a controlled temperature of (22±2)℃ and a 12h light / dark cycle (7:00 / 19:00). After 7 days of acclimatization, the mice were randomly divided into three groups: a blank control group, a model control group, and a Wangbaihe glycoside B group, with 10 mice in each group.
[0093] (1) Preparation and administration of medicine
[0094] Based on the conversion of the 100μM cell administration dose of Wangbaihe glycoside B to the mouse administration dose: mouse weight 20g, gavage volume 0.2mL, mouse administration dose (mg / kg) = [mass concentration (g / L) × administration volume (L)] / animal weight (g), dissolved in DMSO, administered by gavage once daily for 8 weeks.
[0095] (2) Mouse skin photoaging model
[0096] After removing hair from the backs of mice with depilatory cream and wiping them clean, they were randomly divided into three groups after 7 days of acclimatization: a blank control group, a model control group, and a lily glycoside B group, with 10 mice in each group. The blank control group received no treatment, while the model control group received UVA irradiation at 20 J / cm². 2 Five times a week for eight weeks; Group B of Wangbaihegan received UVA irradiation: 20 J / cm². 2 Five times a week for eight weeks, while administering 0.44 mg / kg of Wanglihe glycoside B via gavage daily.
[0097] (3) Observation and photography
[0098] Take photos and record observations of the aging changes in the skin on the backs of mice in each experimental group.
[0099] (4) Skin photoaging classification
[0100] Level 0: No wrinkles;
[0101] Grade I: Mild, mild photoaging, mild pigmentation changes, no seborrheic keratosis, very mild wrinkles;
[0102] Grade II: Moderate photoaging, early brownish solar freckle-like appearance, gradually raised, mild keratosis can be felt, but the appearance of the protrusion is not obvious;
[0103] Grade III: Severe photoaging, with obvious uneven skin color, telangiectasia, and seborrheic keratosis;
[0104] Grade IV: Extremely severe photoaging, characterized by wrinkles and changes in skin texture.
[0105] (5) Data Analysis
[0106] Using Prism software for graphing and data analysis, p < 0.05 was considered statistically significant between groups.
[0107] Table 6. Effects of each experimental group on UVA-induced photoaging grading of dorsal skin in C57BL / 6 mice.
[0108]
[0109] Combined with Table 6 and Figure 5 The results show that the blank control group mice had the lowest degree of photoaging on their backs; compared with the blank control group mice, the model control group mice had a significantly increased degree of photoaging on their backs; and compared with the model control group, the Wangbaihe glycoside B group could significantly improve the aging phenotype of the back skin of mice and significantly reduce the degree of photoaging on the back skin of mice.
[0110] Example 5: Investigating the relative expression levels of type I collagen (COL1A1) and type III collagen (COL3A1) mRNA in the dorsal skin of UVA-induced C57BL / 6 mice by lily glycoside B.
[0111] (1) Preparation and administration of medicine
[0112] Same as described in Example 4.
[0113] (2) Mouse skin photoaging model
[0114] Same as described in Example 4.
[0115] (3) Real-time quantitative PCR
[0116] A 0.5 × 0.5 cm piece of skin tissue was taken from the back of a C57BL / 6 mouse. 2 The RNA was homogenized and lysed in an RNA isolater. 1 / 5 volume of chloroform was added, the mixture was vigorously vortexed, and allowed to stand at room temperature. After centrifugation, the supernatant was transferred, and an equal volume of pre-chilled isopropanol was added. The mixture was allowed to stand at room temperature, centrifuged again, and the supernatant was discarded. The RNA precipitate was washed with pre-chilled 75% ethanol and air-dried at room temperature. The RNA was then dissolved in an appropriate volume of DEPC water to quantify the concentration of the extracted RNA. Reverse transcription was then performed to obtain cDNA, which was used as a template for subsequent amplification. The amplification system consisted of: 0.5 μL cDNA, 2 μL primer mixture (containing upstream and downstream primers), 5 μL 2×ChamQ Universal SYBR qPCR Master Mix, and 2.5 μL ddH2O. Primer sequences are shown in Table 7.
[0117] Table 7 Primer Sequences
[0118]
[0119] Please see Table 8 for detailed experimental results. Figures 6a-6b As shown.
[0120] Table 8. Relative mRNA expression levels of aging-related genes in fibroblasts of each experimental component
[0121]
[0122] Note: Graphing and data analysis were performed using Prism software. A p < 0.05 was considered statistically significant between groups; *** indicates a comparison with the blank control group, p < 0.001; ## indicates a comparison with the model control group, p < 0.01.
[0123] Combined with Table 8 and Figures 6a-6b The results show that lily glycoside B can significantly increase the relative mRNA expression levels of type I collagen gene COL1A1 and type III collagen gene COL3A1 in the dorsal skin of mice induced by UVA.
[0124] The experimental results above show that: Wangbai glycoside B can significantly improve the cell viability of UVA-induced human skin fibroblasts, reduce the number of β-galactosidase-positive cells and decrease lipofuscin deposition in UVA-induced human skin fibroblasts, significantly improve UVA-induced photoaging of skin fibroblasts, and significantly improve the skin aging phenotype on the back of C57BL / 6 mice induced by UVA. It can also increase the relative mRNA expression levels of type I collagen gene COL1A1 and type III collagen gene COL3A1. Therefore, Wangbai glycoside B is expected to be used as an active ingredient in pharmaceuticals or cosmetics for the prevention and / or treatment of photoaging diseases, especially for the prevention and / or treatment of UVA-induced photoaging diseases, which has significant importance and application value.
[0125] Finally, it should be noted that the above should not be construed as a limitation on the scope of protection of this invention. Any non-essential improvements and adjustments made by those skilled in the art based on the above content of this invention shall fall within the scope of protection of this invention.
Claims
1. An application of lily glycoside B, characterized in that: The application refers to the use of lily glycoside B as the sole active ingredient or one of the active ingredients in the preparation of products for the prevention and / or treatment of photoaging skin diseases.
2. The application according to claim 1, characterized in that: The photoaging is UVA-induced photoaging.
3. The application according to claim 1, characterized in that: The aforementioned photoaging skin diseases include at least one of actinic keratosis, squamous cell carcinoma, and malignant melanoma.
4. The application according to claim 1, characterized in that: The product in question is either a cosmetic or a pharmaceutical.
5. The application according to claim 4, characterized in that: The cosmetics mentioned are skincare products or cosmetics containing skincare functions.
6. The application according to claim 4, characterized in that: The dosage forms of the cosmetics include at least one of the following: liquid, emulsion, cream, ointment, gel, patch, and spray.
7. The application according to claim 4, characterized in that: The medicine also includes pharmaceutically acceptable excipients.
8. The application according to claim 7, characterized in that: The pharmaceutically acceptable excipients include at least one of the following: diluents, binders, wetting agents, lubricants, disintegrants, solvents, emulsifiers, cosolvents, solubilizers, preservatives, pH adjusters, osmotic pressure adjusters, surfactants, coating materials, antioxidants, antibacterial agents, and buffers.
9. The application according to claim 4, characterized in that: The dosage form of the medicine includes at least one of granules, capsules, powders, tablets, pills, emulsions, suspensions, syrups, ointments, injections, suppositories, aerosols, gels, patches, and drops.
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