Topical formulation for treating atopic dermatitis, preparation method therefor, and use thereof
Patent Information
- Authority / Receiving Office
- WO · WO
- Patent Type
- Applications
- Current Assignee / Owner
- Filing Date
- 2025-06-05
- Publication Date
- 2026-08-13
Smart Images
Figure CN2025099255_13082026_PF_FP_ABST
Abstract
Description
A topical preparation for treating atopic dermatitis, its preparation method and application.
[0001] This application claims priority to Chinese Patent Application No. 202510131320.9, filed on February 6, 2025, entitled "A topical preparation for treating atopic dermatitis and its preparation method and application", the entire contents of which are incorporated herein by reference. Technical Field
[0002] This application belongs to the field of traditional Chinese medicine external preparation development technology, and in particular relates to an external preparation for treating atopic dermatitis, its preparation method and application. Background Technology
[0003] Atopic dermatitis (AD) is a chronic, relapsing, inflammatory skin disease characterized by dry skin, chronic eczematous dermatitis, and intense itching. Because patients often have other atopic diseases such as allergic rhinitis and asthma, and approximately 40%-80% of patients have a family history of allergies, it is considered a systemic disease. The pathogenesis of AD is influenced by multiple factors, resulting from the interaction of genetic, immune, infectious, and environmental factors. Current treatments for AD primarily involve topical corticosteroids, topical calcineurin inhibitors, oral antihistamines, systemic immunosuppressants, and corticosteroids. These medications have good short-term therapeutic effects on atopic dermatitis, but long-term use has significant side effects and a high relapse rate. For example, corticosteroids are the first-line treatment for AD and are often the first-line drug, but long-term topical corticosteroid use may cause side effects such as skin atrophy, telangiectasia, striae, purpura, and hirsutism.
[0004] Traditional Chinese medicine (TCM) topical medications have shown certain advantages in improving clinical symptoms and reducing recurrence rates in patients with mild to severe atopic dermatitis. In a randomized, double-blind clinical trial, indigo naturalis ointment effectively reduced the severity of skin lesions and itching while ensuring safety. Multiple studies have found that TCM topical agents can improve skin lesions in AD mice and reduce inflammatory markers in serum and skin lesions. Licorice has the effects of clearing heat and detoxifying, relieving spasms and pain, and possesses anti-inflammatory, anti-tumor, antibacterial, and immunomodulatory pharmacological effects. It is widely used in dermatology. Its main component, glycyrrhizin, has been shown to have various pharmacological activities such as anti-inflammatory, antioxidant, and apoptosis-inhibiting effects, and can be used to treat various skin diseases, such as photoaging and psoriasis. Neoglycyrrhizin, as one of the active ingredients of licorice, has also been proven to have strong anti-inflammatory and antiviral effects. Summary of the Invention
[0005] In view of this, the purpose of this application is to provide a topical preparation for treating atopic dermatitis, its preparation method and application, which uses neoglycyrrhizin as the active ingredient to treat atopic dermatitis and has a significant effect, thus expanding the application field of neoglycyrrhizin.
[0006] To address the aforementioned technical problems, this application provides the following technical solutions:
[0007] This application provides a topical preparation for treating atopic dermatitis, the active ingredient of which is neoglycyrrhizin.
[0008] This application provides a cream for treating atopic dermatitis, comprising the following components by mass concentration: 0.5%-1.5% neoglycyrrhizin, 4%-13% solvent, 5%-25% oil phase, 56%-87% aqueous phase, 2%-8% emulsifier, and 0.05%-0.15% preservative.
[0009] This application provides a method for preparing a cream for treating atopic dermatitis, comprising the following steps: (1) weighing an oil phase, an emulsifier and a preservative as a first mixture, weighing an aqueous phase as a second mixture, and dissolving neoglycyrrhizin in a solvent as a third mixture; (2) heating and mixing the first mixture and the second mixture, homogenizing them, and then adding the third mixture and homogenizing again; (3) cooling to obtain the cream.
[0010] This application also provides the use of the aforementioned topical formulation in the preparation of a drug for treating atopic dermatitis and in the preparation of a drug for inhibiting epidermal proliferation and / or dermal lymphocyte infiltration. Attached Figure Description
[0011] Figure 1 shows the effect of neoglycyrrhizin solution on the activity of HaCaT cells; in the figure, a is the chemical structural formula of neoglycyrrhizin; b is the effect of different concentrations of neoglycyrrhizin solution on the proliferation activity of HaCaT cells; c is the effect of 2 μM and 10 μM concentrations of neoglycyrrhizin solution on the expression of inflammatory factors IL-4 and IL-13 mRNA in HaCaT cells.
[0012] Figure 2 shows the skin lesions and dermatitis scores of different drug groups in a mouse model of atopic dermatitis; in the figure, a is a typical photograph of the auricular skin lesions and changes in the skin lesions of mice in different drug groups (Day 12) (n=5); b is the auricular thickness of mice in different drug groups (n=5); c is the EASI score of the skin lesions of mice in different drug groups (n=5).
[0013] Figure 3 shows the histopathological findings of different drug-treated mouse models of atopic dermatitis; in the figure, a represents the histopathological changes of the auricle tissue of mice in different drug-treated groups (×100) (n=5); b represents the epidermal thickness of the auricle of mice in different drug-treated groups (n=5); c represents the quantitative comparison of the number of dermal lymphocytes in mice in different drug-treated groups (n=5).
[0014] Figure 4 shows the pathological changes in the liver, spleen, and kidneys of mice when neoglycyrrhizin was applied topically (×200);
[0015] Note: In Figures 1-3, compared to the model group... ** p<0.01, *** p<0.001; compared with the normal control group, ## p<0.01, ### p<0.001. Detailed Implementation
[0016] This application provides a topical preparation for treating atopic dermatitis, the active ingredient of which is neoglycyrrhizin.
[0017] Neoglycyrrhizin is a flavonoid compound commonly found in the medicinal parts of licorice, a legume. It possesses various pharmacological activities, including anti-inflammatory and antiviral effects. Its chemical structure is shown in Figure 1a, and its molecular formula is C1. 21 H 22 O9, molecular weight 418.4, CAS number 5088-75-5.
[0018] In this application, the concentration of neoglycyrrhizin is preferably 0.5wt%-1.5wt%, more preferably 0.8wt%-1.5wt%, and even more preferably 1wt%.
[0019] In this application, preferred dosage forms of topical preparations include patches, pastes, ointments, creams, gels, oils, microneedles, films, poultices, sprays, and dressings; further preferred are topical preparations that also include pharmaceutically acceptable excipients. This invention does not impose any particular limitations on the preparation methods of excipients and topical preparations; commonly used excipients and conventional preparation methods in the pharmaceutical field are sufficient.
[0020] This application also provides a cream for treating atopic dermatitis, comprising the following components by mass concentration: 0.5%-1.5% neoglycyrrhizin, 4%-13% solvent, 5%-25% oil phase, 56%-87% aqueous phase, 2%-8% emulsifier, and 0.05%-0.15% preservative; more preferably, 0.8%-1.2% neoglycyrrhizin, 6%-10% solvent, 10%-20% oil phase, 65%-75% aqueous phase, 3%-5% emulsifier, and 0.08%-0.12% preservative; more preferably, 1% neoglycyrrhizin, 8.3% solvent, 14.0% oil phase, 71.9% aqueous phase, 4.7% emulsifier, and 0.1% preservative.
[0021] In this application, the solvent is preferably selected from one or more of diethylene glycol monoethyl ether, ethanol, and propylene glycol; more preferably, it is diethylene glycol monoethyl ether.
[0022] The preferred oil phase is selected from one or more of glyceryl monostearate and glyceryl distearate, cetearyl alcohol, liquid paraffin, petrolatum, and lanolin; more preferably, glyceryl monostearate and glyceryl distearate, cetearyl alcohol, and liquid paraffin; even more preferably, glyceryl monostearate and glyceryl distearate: cetearyl alcohol: liquid paraffin = 3:5:6.
[0023] The preferred aqueous phase is selected from one or more of pure water, deionized water, and glycerol; more preferably, it is pure water and glycerol; even more preferably, it is pure water:glycerol = 9.3:1.
[0024] The preferred emulsifier is selected from one or more of polyethylene glycol-7-stearate, polyoxyethylene (21) stearyl alcohol ether, polyoxyethylene (2) stearyl alcohol ether, polyglycerol oleate, and sodium lauryl sulfate; more preferably, polyethylene glycol-7-stearate, polyoxyethylene (21) stearyl alcohol ether, polyoxyethylene (2) stearyl alcohol ether, and polyglycerol oleate; more preferably, polyethylene glycol-7-stearate: polyoxyethylene (21) stearyl alcohol ether: polyoxyethylene (2) stearyl alcohol ether: polyglycerol oleate = 4:9:9:6.
[0025] The preferred preservative is selected from one or more of ethylparaben, methylparaben, and phenoxyethanol; ethylparaben is more preferred.
[0026] This application also provides a method for preparing the above-mentioned cream for treating atopic dermatitis, comprising the following steps:
[0027] (1) Weigh out the oil phase, emulsifier and preservative to make the first mixture, weigh out the aqueous phase to make the second mixture, and dissolve the neoglycyrrhizin in the solvent to make the third mixture;
[0028] (2) After heating and mixing the first mixture and the second mixture and homogenizing them, the third mixture is added and homogenized again; preferably, the first mixture and the second mixture are heated to 85°C and then mixed, homogenized for 3 min, cooled to 60°C, and the third mixture is added and homogenized again for 3 min.
[0029] (3) The cream is obtained by cooling, preferably by cooling to 40°C and then dispensing.
[0030] This application also provides the use of the aforementioned topical preparation in the preparation of drugs for treating atopic dermatitis and in the preparation of drugs for inhibiting epidermal proliferation and / or dermal lymphocyte infiltration.
[0031] This application has the following beneficial effects:
[0032] This application uses neoglycyrrhizin as the active ingredient in a topical preparation for the treatment of atopic dermatitis, providing a new option for the treatment of atopic dermatitis and offering several significant advantages.
[0033] In terms of safety, neoglycyrrhizin has no adverse effects on the normal growth of skin cells and exhibits good safety, providing an important prerequisite for its topical treatment. When applied topically, it has no significant toxic side effects on vital organs. Compared to traditional treatments such as long-term topical corticosteroids, which may cause skin atrophy, telangiectasia, stretch marks, purpura, and hirsutism, neoglycyrrhizin demonstrates a significant safety advantage, reducing the risk of adverse reactions to drug treatment for patients.
[0034] From a therapeutic perspective, neoglycyrrhizin can effectively intervene in the inflammatory response process of atopic dermatitis at the cellular level, fundamentally regulating immune-related inflammatory signaling pathways and laying the foundation for alleviating skin inflammation. Neoglycyrrhizin has a significant effect on improving the skin symptoms of atopic dermatitis, effectively reducing symptoms such as inflammation, erythema, edema, and scaling, and improving the health of the skin. Neoglycyrrhizin can also effectively regulate the pathological structure of skin tissue, promote skin tissue repair and normalization, and enhance the skin's barrier function and immune homeostasis.
[0035] The formulation design of the new glycyrrhizin cream in this application ensures the stability, efficacy, and safety of the preparation, enabling the drug to exert its therapeutic effect better, improving the bioavailability and duration of efficacy, and providing a reliable formulation basis for clinical application.
[0036] The present application will be further described below with reference to the accompanying drawings and embodiments.
[0037] Unless otherwise specified, the methods used in the following embodiments are conventional methods.
[0038] Example 1
[0039] A topical cream for treating atopic dermatitis, prepared as follows:
[0040] (1) Weigh out 36g of mono- and di-stearate glyceryl esters, 60g of cetearyl alcohol, 72g of liquid paraffin, 1.2g of ethylparaben, 8g of polyethylene glycol-7-stearate, 18g of polyoxyethylene (21) stearyl alcohol ether, 18g of polyoxyethylene (2) stearyl alcohol ether, and 12g of polyglycerol oleate as component A.
[0041] (2) Weigh 1978.8g of pure water and 84g of glycerol as component B;
[0042] (3) Weigh 100g of diethylene glycol monoethyl ether and add 12g of neoglycyrrhizin, and sonicate for 30min to fully dissolve it as component C.
[0043] (4) Heat components A and B to 85°C and mix them thoroughly with stirring, then homogenize for 3 minutes.
[0044] (5) When the mixture of A and B drops to about 60°C, add component C and continue homogenizing for 3 minutes;
[0045] (6) The sample is dispensed when it is cooled to about 40°C.
[0046] Example 2
[0047] A topical cream for treating atopic dermatitis, prepared as follows:
[0048] (1) Weigh out 36g of mono- and di-stearate glyceryl esters, 60g of cetearyl alcohol, 72g of liquid paraffin, 1.2g of ethylparaben, 8g of polyethylene glycol-7-stearate, 18g of polyoxyethylene (21) stearyl alcohol ether, 18g of polyoxyethylene (2) stearyl alcohol ether, and 12g of polyglycerol oleate as component A.
[0049] (2) Weigh 778.8g of pure water and 84g of glycerol as component B;
[0050] (3) Weigh 100g of diethylene glycol monoethyl ether and add 12g of neoglycyrrhizin, and sonicate for 30min to fully dissolve it as component C.
[0051] (4) Heat components A and B to 85°C and mix them thoroughly with stirring, then homogenize for 3 minutes.
[0052] (5) When the mixture of A and B drops to about 60°C, add component C and continue homogenizing for 3 minutes;
[0053] (6) The sample is dispensed when it is cooled to about 40°C.
[0054] Example 3
[0055] A topical cream for treating atopic dermatitis, prepared as follows:
[0056] (1) Weigh out 36g of mono- and di-stearate glyceryl esters, 60g of cetearyl alcohol, 72g of liquid paraffin, 1.2g of ethylparaben, 8g of polyethylene glycol-7-stearate, 18g of polyoxyethylene (21) stearyl alcohol ether, 18g of polyoxyethylene (2) stearyl alcohol ether, and 12g of polyglycerol oleate as component A.
[0057] (2) Weigh out 378.8g of pure water and 84g of glycerol as component B;
[0058] (3) Weigh 100g of diethylene glycol monoethyl ether and add 12g of neoglycyrrhizin, and sonicate for 30min to fully dissolve it as component C.
[0059] (4) Heat components A and B to 85°C and mix them thoroughly with stirring, then homogenize for 3 minutes.
[0060] (5) When the mixture of A and B drops to about 60°C, add component C and continue homogenizing for 3 minutes;
[0061] (6) The sample is dispensed when it is cooled to about 40°C.
[0062] Example 4
[0063] HaCaT cell viability assay
[0064] Weigh 20 mg of neoglycyrrhizin, dissolve it in PBS after sonication, and prepare a stock solution with a final concentration of 50.00 mM according to the minimum solubility of DMSO. Store it in a refrigerator at 4°C for subsequent experiments.
[0065] Cell culture and treatment: HaCaT cells were purchased from Cell Lines Service (Eppelheim, 300493) and cultured in DMEM medium containing 10% fetal bovine serum. The cell lines were passaged three times in a 37°C incubator with 5% CO2 before subsequent experiments.
[0066] (1) HaCaT cell viability detection
[0067] The experiment using the neoglycyrrhizin solution was divided into a blank control group and different concentration groups of 2, 5, 10, 20, and 50 μM, with four replicates in each group. HaCaT cells were seeded into 96-well plates. When the cells reached over 80% confluence, the original culture medium was discarded, and 0.1 mL of culture medium containing different concentrations of the drug was added to each well. The blank control group was treated with complete culture medium without the drug. The plates were then incubated for further culture. 48 h after neoglycyrrhizin treatment, the original culture medium was discarded, and the cells were washed once with 100 μL of PBS buffer per well. 110 μL of CCK-8 working solution (prepared at a CCK-8 reagent: complete cell culture medium ratio of 1:10) was added to each well. The plates were incubated for another 2 h. Subsequently, the absorbance of the 96-well plates was read at 450 nm using a multi-mode microplate reader, and the cell viability was calculated based on the absorbance values.
[0068] The results are shown in Figure 1b. The effect of different concentrations of neoglycyrrhizin on the proliferation activity of HaCaT cells was detected using CCK-8 assays to screen the effective in vitro concentration of neoglycyrrhizin for subsequent experiments. Specifically, after treatment with 2, 5, 10, 20, and 50 μM neoglycyrrhizin solutions for 48 h, the cell proliferation rate was not significantly different from the control group. This indicates that 2 to 50 μM neoglycyrrhizin solutions did not inhibit HaCaT cell proliferation, and also suggests that this monomeric component has good safety.
[0069] (2) RT-qPCR was performed on TSLP-stimulated HaCaT cells using 2 μM and 10 μM neoglycyrrhizin solutions, respectively, to detect its effect on the mRNA of inflammatory factors IL-4 and IL-13. The specific methods are as follows:
[0070] Cells were cultured in 6-well plates, divided into a blank control group (NC) and groups with different drug concentrations (0, 2, 10 μM), with four replicates in each group. When HaCaT cells reached approximately 70% confluence, human thymic stromal lymphopoietin (TSLP) was added to the complete culture medium at a predetermined concentration (100 ng / mL) to simulate the inflammatory environment of atopic dermatitis. TSLP was then mixed with 2 mL of different concentrations of neoglycyrrhizin solution and added to the culture medium to stimulate the cells for 48 h.
[0071] Total mRNA was extracted from HaCaT cells using the Trizol method (Beyotime, Shanghai, China). RNA concentration and purity were determined by measuring the absorbance 260 / 280 ratio using a UV spectrophotometer. cDNA was prepared using a reverse transcription kit and reverse transcribed using reverse transcriptase. Two [units of technology were used]. -ΔΔCT Methods were used to analyze relative quantitative data. Polymerase chain reaction primers are shown in Table 1.
[0072] Table 1 Polymerase Chain Reaction Primers
[0073] The results are shown in Figure 1c. The mRNA expression of inflammatory factors IL-4 and IL-13 in HaCaT cells decreased at both 2 μM and 10 μM concentrations, with the most significant decrease at 10 μM (compared to the TSLP group). * p<0.05, ** p<0.01).
[0074] Example 5
[0075] Atopic dermatitis mouse model experiment
[0076] 1. Drug preparation: Prepared according to Examples 1 to 3.
[0077] 2. Experimental Methods
[0078] 2.1. Group intervention
[0079] Male C57BL / 6 mice, aged 6-8 weeks and weighing 20g±2g, were randomly divided into 6 groups of 5 mice each. The mice were housed in a specific sterile environment with temperature control (20-26℃) and provided with standard feed and water. The grouping and treatment protocols are as follows:
[0080] (1) Normal control group: Apply 20 μL of anhydrous ethanol to the inner and outer sides of the two auricles of mice daily for 5 days, stop for 2 days, and then apply for another 5 days.
[0081] (2) Model group: The inner and outer sides of the two auricles of mice were coated daily with 20 μL of calcipotriol (MC903) ethanol solvent containing 2 nmol for 5 days, then stopped for 2 days, and then coated for another 5 days.
[0082] (3) 0.5wt% neoglycyrrhizin group: The inner and outer sides of the mouse auricles were coated daily with 20 μL of calcipotriol (MC903) ethanol solvent containing 2 nmol. After 6 hours, 5 mg of 0.5% neoglycyrrhizin cream prepared in Example 1 was applied to the inner and outer sides of the mouse auricles. The application was repeated for 12 days.
[0083] (4) 1.0wt% neoglycyrrhizin group: The inner and outer sides of the two auricles of mice were coated daily with 20μL of calcipotriol (MC903) ethanol solvent containing 2 nmol. After 6 hours, 5 mg of 1.0% neoglycyrrhizin cream prepared in Example 2 was applied to the inner and outer sides of the two auricles of mice. The application was repeated for a total of 12 days.
[0084] (5) 1.5wt% neoglycyrrhizin group: The inner and outer sides of the mouse auricles were coated daily with 20 μL of calcipotriol (MC903) ethanol solvent containing 2 nmol. After 6 hours, 5 mg of 1.5% neoglycyrrhizin cream prepared in Example 3 was applied to the inner and outer sides of the mouse auricles. The application was repeated for 12 days.
[0085] All treatments began on day 1 of calcipotriol administration. All animal studies were approved by the Ethics Committee of Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, affiliated with Shanghai University of Traditional Chinese Medicine.
[0086] 2.2. Observation Indicators
[0087] The appearance of the mouse ears was photographed on days 1, 5, 8, and 12. The thickness of the ear skin at the same location was measured with calipers and the values were recorded. The severity of the ear skin inflammation in mice was scored according to the Area and Severity Index (EASI) of Atopic Dermatitis, which includes four parts: erythema, edema or exudation, scaling, and lichenification. The scores represent the severity: 0 (none), 1 (mild), 2 (moderate), and 3 (severe).
[0088] 3. Histopathology
[0089] After recording the above data on day 12, the mice were euthanized, and 1×1cm skin tissue was taken from both ears of each group of mice. The tissue was fixed in 4% formalin solution for 48 hours, embedded in paraffin, sectioned, and stained with hematoxylin-eosin (H&E). The epidermal thickness was measured in four high-power fields of each section, and the average value was taken.
[0090] 4. Statistical Methods
[0091] Experimental data were analyzed using GraphPad Prism 9, and all data are expressed as mean ± standard deviation (SD). Multiple comparisons between groups were performed using one-way ANOVA and Tukey ANOVA. A p-value <0.05 was considered statistically significant.
[0092] 5. Experimental Results
[0093] 5.1. Neoglycyrrhizin can improve skin lesions and dermatitis scores in a mouse model of calcipotriol-induced atopic dermatitis.
[0094] Typical photographs and lesion details of the auricle skin in each group of mice are shown in Figure 2a. The study found that calcipotriol-induced auricular skin thickness in mice (model group) was significantly increased. ### p<0.001), the ear thickness was significantly reduced in the 1.0wt% neoglycyrrhizin group and the 1.5wt% neoglycyrrhizin group compared with the MC903 group. * p<0.05, ** p<0.01 (Figure 2b). There was no significant difference in ear skin thickness between the 0.5wt% neoglycyrrhizin group and the MC903 group. The EASI score was significantly higher in the model group than in the normal control group. ### p<0.001), the three concentrations of neoglycyrrhizin were significantly lower than those in the model group. ** p<0.01, *** p<0.001 (Figure 2c). The results above show that both 1.0 wt% neoglycyrrhizin and 1.5 wt% neoglycyrrhizin can improve the appearance of skin lesions and ear thickness in AD-like mice, and the efficacy of the 1.0 wt% neoglycyrrhizin group is better than that of the 1.5 wt% neoglycyrrhizin group.
[0095] 5.2. Neoglycyrrhizin can improve the histopathological condition of mice with calcipotriol-induced atopic dermatitis.
[0096] Based on the above results, three concentrations of neoglycyrrhizin were selected for further research. The results showed that at 12 days, the skin lesions in mice treated with the three concentrations of neoglycyrrhizin were significantly improved compared to the model group (Figure 3). Histopathological sections of the mice in each group (Figure 3a, scale bar = 250 μm) showed that the model group exhibited epidermal hyperplasia, dermal inflammatory cell infiltration, and acanthosis; all three concentrations of neoglycyrrhizin showed slight epidermal thickening, less dermal inflammatory cell infiltration, and less significant acanthosis, with the 1.0 wt% neoglycyrrhizin group showing more significant improvement. Furthermore, ImageJ quantification showed that the epidermal thickness in the model group was significantly higher than that in the normal control group (Figure 3). ###p<0.001); the epidermal thickness of the three concentrations of glycyrrhizin groups was significantly reduced compared with the model group. *** p<0.001 (Figure 3b). Meanwhile, the number of skin lymphocytes was significantly higher in the model group compared to the normal control group (p<0.001). ### p<0.001); the number of skin lymphocytes in the three concentrations of glycyrrhizin groups was significantly lower than that in the model group. *** p<0.001 (Figure 3c). The 1.0wt% neoglycyrrhizin group was superior to the 0.5wt% and 1.5wt% neoglycyrrhizin groups in terms of epidermal thickness and skin lymphocyte count, and further safety studies will be conducted.
[0097] 5.3. Topical application of neoglycyrrhizin had no effect on the liver, spleen, and kidneys of mice with calcipotriol-induced atopic dermatitis.
[0098] Histopathological sections of liver, spleen and kidney tissues from mice in each group (Figure 4, scale bar = 100 μm) showed no significant difference between the normal control group and the 1.0 wt% neoglycyrrhizin group, proving that neoglycyrrhizin did not produce toxic side effects on the liver, spleen and kidneys during treatment.
[0099] The novel glycyrrhizin, a single herb in this application, can significantly reduce skin erythema, dryness, scratches, and epidermal erosion and peeling in infected mice, demonstrating remarkable efficacy and making it worthy of promotion.
[0100] The above description is only a preferred embodiment of this application. It should be noted that for those skilled in the art, several improvements and modifications can be made without departing from the principle of this application, and these improvements and modifications should also be considered within the scope of protection of this application.
Claims
1. A topical preparation for treating atopic dermatitis, characterized in that, The active ingredient in the topical preparation is neoglycyrrhizin.
2. The topical preparation according to claim 1, characterized in that, The concentration of the neoglycyrrhizin is 0.5wt%-1.5wt%.
3. The topical preparation according to claim 1, characterized in that, The concentration of the neoglycyrrhizin is 1 wt%.
4. The topical preparation according to any one of claims 1-3, characterized in that, The dosage forms of the topical preparations include patches, pastes, ointments, creams, gels, oils, microneedles, films, poultices, sprays, and dressings.
5. The topical preparation according to claim 4, characterized in that, The topical preparation also includes pharmaceutically acceptable excipients.
6. A cream for treating atopic dermatitis, characterized in that, The components, by mass concentration, include: neoglycyrrhizin 0.5%-1.5%, solvent 4%-13%, oil phase 5%-25%, aqueous phase 56%-87%, emulsifier 2%-8%, and preservative 0.05%-0.15%.
7. The cream according to claim 6, characterized in that, The components, by mass concentration, include: neoglycyrrhizin 0.8%-1.2%, solvent 6%-10%, oil phase 10%-20%, aqueous phase 65%-75%, emulsifier 3%-5%, and preservative 0.08%-0.12%.
8. The cream according to claim 6, characterized in that, The components, by mass concentration, include: 1% neoglycyrrhizin, 8.3% solvent, 14.0% oil phase, 71.9% aqueous phase, 4.7% emulsifier, and 0.1% preservative.
9. The cream according to any one of claims 6-8, characterized in that, The solvent is selected from one or more of diethylene glycol monoethyl ether, ethanol, and propylene glycol.
10. The cream according to any one of claims 6-8, characterized in that, The oil phase is selected from one or more of the following: glyceryl monostearate and glyceryl distearate, cetearyl alcohol, liquid paraffin, petrolatum, and lanolin.
11. The cream according to claim 10, characterized in that, The oil phase consists of glyceryl monostearate and glyceryl distearate, cetearyl alcohol, and liquid paraffin in a mass ratio of 3:5:
6.
12. The cream according to any one of claims 6-8, characterized in that, The aqueous phase is selected from one or more of pure water, deionized water, and glycerol.
13. The cream according to claim 12, characterized in that, The aqueous phase consists of pure water and glycerol in a mass ratio of 9.3:
1.
14. The cream according to any one of claims 6-8, characterized in that, The emulsifier is selected from one or more of polyethylene glycol-7-stearate, polyoxyethylene (21) stearyl alcohol ether, polyoxyethylene (2) stearyl alcohol ether, polyglycerol oleate, and sodium dodecyl sulfate.
15. The cream according to claim 14, characterized in that, The emulsifier is polyethylene glycol-7-stearate, polyoxyethylene (21) stearyl alcohol ether, polyoxyethylene (2) stearyl alcohol ether and polyglycerol oleate, in a mass ratio of 4:9:9:
6.
16. The cream according to any one of claims 6-8, characterized in that, The preservative is selected from one or more of ethylparaben, methylparaben, and phenoxyethanol.
17. A method for preparing the cream according to any one of claims 6-8, characterized in that, Includes the following steps: (1) Weigh the oil phase, emulsifier and preservative to form the first mixture, weigh the aqueous phase to form the second mixture, and dissolve the neoglycyrrhizin in the solvent to form the third mixture; (2) Heat and mix the first mixture and the second mixture, then add the third mixture and homogenize again; (3) Cool to obtain the cream.
18. The preparation method according to claim 17, characterized in that, In step (2), the first mixture and the second mixture are heated to 85°C and then mixed, homogenized for 3 minutes, cooled to 60°C, and the third mixture is added and homogenized again for 3 minutes.
19. The use of the topical preparation according to any one of claims 1-3 in the preparation of a medicament for treating atopic dermatitis.
20. The use of the topical formulation according to any one of claims 1-3 in the preparation of a medicament for inhibiting epidermal proliferation and / or dermal lymphocyte infiltration.