A cosmetic capsaicin stimulation inhibitor, and a preparation method and application thereof

Abstract

The application discloses a capsaicin stimulation inhibitor for cosmetics and a preparation method and application thereof. The preparation method of the capsaicin stimulation inhibitor for cosmetics comprises the following steps: A, soaking medicinal materials with 15-20 times weight of extraction solvent for 2-16 hours to obtain a soaking solution; the extraction solvent is an alkali aqueous solution with a concentration of 0.2-0.8 mol / L, and the medicinal materials are at least one of calendula, spade heron and radix scrophulariae; B, extracting the soaking solution at 95-105 DEG C for 1-3 hours. The capsaicin stimulation inhibitor for cosmetics prepared by the preparation method can significantly inhibit the secretion of IL-1 alpha of keratinocytes and the expression of TRPV-1 protein caused by capsaicin stimulation, and the combinations have certain synergies, so that the capsaicin stimulation inhibitor for cosmetics can be applied to the inhibition of TRPV1 expression induced by capsaicin, the inhibition of IL-1 alpha secretion induced by capsaicin and the preparation of skin external preparation.

Description

TECHNICAL FIELD

[0001] The present application belongs to the field of biotechnology, and particularly relates to a cosmetic capsaicin stimulation inhibitor and a preparation method and application thereof. BACKGROUND

[0002] TRPV1, full name Transient Receptor Potential Vanilloid 1, is a non-selective cation channel belonging to the vanilloid subfamily of the transient receptor potential (TRP) ion channel family. It was first discovered as a capsaicin receptor, so it is also called capsaicin receptor or vanilloid receptor 1. TRPV1 can be activated by various physical and chemical stimuli, such as high temperature (> 43℃), endogenous lipid molecules and exogenous ligands, and is involved in pain perception, temperature regulation, inflammatory response and other physiological and pathological processes. TRPV1 is one of the target points most closely related to skin burning, stinging and other allergic reactions in the field of cosmetics. By screening plant extracts and their combinations that inhibit the expression of TRPV1, it is an important means to develop anti-irritation and anti-allergic agents for cosmetics. Based on this technical means, the present application screens different plants and process extracts, and finds plant extracts and their combinations with specific anti-allergic effects.

[0003] The expression of TRPV1 in sensitive skin is significantly increased, resulting in more sensitive skin to various stimuli, producing stinging, itching and other discomfort. Therefore, the use of skin care products that can inhibit the expression of TRPV1 receptor is very important for relieving the symptoms of sensitive skin. Secondly, TRPV1 is involved in the occurrence and development of various inflammatory skin diseases. Activation of TRPV1 can lead to the release of neuropeptides or pro-inflammatory mediators, such as prostaglandin E2 (PGE2), interleukins and other inflammatory factors related to skin inflammatory response, inducing the occurrence and development of skin inflammation. In summary, TRPV1 has important significance in the research of skin care products. It is not only related to the relief of sensitive skin symptoms, but also involved in the treatment and link of inflammatory skin diseases. Therefore, developing skin care ingredients with TRPV1 as a target is expected to be a new solution for sensitive and inflammatory skin care and treatment.

[0004] IL-1α is a pro-inflammatory cytokine secreted by various cells (such as macrophages, monocytes, endothelial cells, keratinocytes, etc.) when stimulated (such as infection, tissue damage, etc.). It mainly exerts biological effects by activating NF-κB and MAPK signaling pathways, thereby inducing the production of other cytokines, promoting the activation and migration of immune cells, and participating in the regulation of inflammatory response and immune response. For example, when the skin is stimulated or damaged, IL-1α can stimulate monocytes, neutrophils and fibroblasts to secrete IL-6, IL-8, TNF-α and other pro-inflammatory cytokines, which further promote the occurrence and development of inflammatory response. In addition, IL-1α can also attract neutrophils and cause the release of inflammatory mediators, thereby exacerbating the inflammatory response.

[0005] In summary, IL-1α is an important pro-inflammatory cytokine that plays an important role in inflammatory response, immune response and tissue repair. Research on the biological effects and clinical applications of IL-1α is of great significance for understanding the pathogenesis of diseases and developing new treatment methods. SUMMARY

[0006] The present application finds that the cosmetic capsaicin stimulation inhibitor prepared by selecting specific ingredients alone, in pairs or in combination of three ingredients can improve the inhibition rate of TRPV1 expression induced by capsaicin and improve the inhibition rate of IL-1α secretion induced by capsaicin. Therefore, the first object of the present application is to provide a preparation method of a cosmetic capsaicin stimulation inhibitor; the second object of the present application is to provide a cosmetic capsaicin stimulation inhibitor prepared by the preparation method of the cosmetic capsaicin stimulation inhibitor described above; the third object of the present application is to provide the application of the cosmetic capsaicin stimulation inhibitor described above in inhibiting the expression of TRPV1 induced by capsaicin. The fourth object of the present application is to provide the application of the cosmetic capsaicin stimulation inhibitor described above in inhibiting the secretion of IL-1α induced by capsaicin.

[0007] To achieve the above-mentioned objects, the present application adopts the following technical solutions:

[0008] As a first aspect of the present application, a preparation method of a cosmetic capsaicin stimulation inhibitor comprises the following steps:

[0009] A. Soak the medicinal materials with 15-20 times the weight of the extraction solvent for 2-16 hours to obtain a soaking solution; the extraction solvent is a 0.2 mol / L-0.8 mol / L aqueous alkali solution, and the medicinal materials are at least one of calendula, spiny amaranth and figwort;

[0010] B. Extract the soaking solution at 95-105℃ for 1-3 hours.

[0011] According to the present application, after step B, further comprising the following steps:

[0012] C, removing filter residue, decoloring, filtering to be clear, desalting, concentrating to extract, and obtaining the cosmetic capsaicin stimulation inhibitor.

[0013] Preferably, the concentration of the aqueous alkali solution is 0.2 mol / L-0.5 mol / L.

[0014] According to the present application, the medicinal materials are two of the following: Calendula officinalis, Herba Portulacae, and Scrophularia ningpoensis, the weight ratio of the Calendula officinalis and Herba Portulacae is 30-50:50-70, or,

[0015] the weight ratio of the Calendula officinalis and Herba Portulacae is 30-50:50-70, or,

[0016] the weight ratio of the Calendula officinalis and Herba Portulacae is 30-50:50-70, or,

[0017] According to the present application, the medicinal materials are Calendula officinalis, Herba Portulacae, and Scrophularia ningpoensis, and the weight ratio of the Calendula officinalis, Herba Portulacae, and Scrophularia ningpoensis is 30:50:20.

[0018] According to the present application, the aqueous alkali solution in step A is one or a combination of the following: aqueous sodium hydroxide solution, aqueous potassium hydroxide solution, aqueous sodium carbonate solution, and aqueous arginine solution. Preferably, the aqueous alkali solution in step A is one or a combination of the following: aqueous sodium hydroxide solution, aqueous potassium hydroxide solution, and aqueous arginine solution; more preferably, the aqueous alkali solution in step A is aqueous arginine solution.

[0019] According to the present application, the decoloring in step C is carried out by activated carbon adsorption decoloring; and / or,

[0020] The desalting in step C is carried out by ion exchange resin desalting.

[0021] As a second aspect of the present application, a cosmetic capsaicin stimulation inhibitor is prepared by the preparation method of the cosmetic capsaicin stimulation inhibitor described above.

[0022] As a third aspect of the present application, the cosmetic capsaicin stimulation inhibitor is used for inhibiting capsaicin-induced TRPV1 expression.

[0023] As a fourth aspect of the present application, the cosmetic capsaicin stimulation inhibitor is used for inhibiting capsaicin-induced IL-1α secretion.

[0024] As a fifth aspect of the present application, the cosmetic capsaicin stimulation inhibitor is used for preparing a skin external preparation, and has an anti-stimulation effect.

[0025] The cosmetic capsaicin stimulation inhibitor, the preparation method and application thereof have the beneficial effects that the cosmetic capsaicin inhibitor can significantly inhibit the secretion of IL-1α of keratinocytes and the expression of TRPV-1 protein caused by capsaicin stimulation, and the combinations have certain synergies; the cosmetic capsaicin inhibitor can be used in external preparations, and has the effect of anti-stimulation. BRIEF DESCRIPTION OF DRAWINGS

[0026] Figure 1 Figure 1 is the cck-8 experimental result graph of Example 1; *p<0.05 vs NC;

[0027] Figure 2 Figure 2 is the cck-8 experimental result graph of Example 2; *p<0.05 vs NC;

[0028] Figure 3 Figure 3 is the cck-8 experimental result graph of Example 3;

[0029] Figure 4 Figure 4 is the cck-8 experimental result graph of Example 4;

[0030] Figure 5 Figure 5 is the cck-8 experimental result graph of Example 5;

[0031] Figure 6 Figure 6 is the cck-8 experimental result graph of Example 6; *p<0.05 vs NC;

[0032] Figure 7 Figure 7 is the cck-8 experimental result graph of Example 7; *p<0.05 vs NC;

[0033] Figure 8 Figure 8 is the cck-8 experimental result graph of Example 8;

[0034] Figure 9 Figure 9 is the cck-8 experimental result graph of Example 9; *p<0.05 vs NC;

[0035] Figure 10 Figure 10 is the cck-8 experimental result graph of Example 10;

[0036] Figure 11 Figure 11 is the cck-8 experimental result graph of Example 11;

[0037] Figure 12 Figure 12 is the cck-8 experimental result graph of Comparative Example 1;

[0038] Figure 13 Figure 13 is the cck-8 experimental result graph of Comparative Example 2;

[0039] Figure 14Figure for cck-8 experiment result of comparative example 3;

[0040] Figure 15 Figure for cck-8 experiment result of comparative example 4;

[0041] Figure 16 Figure for cck-8 experiment result of comparative example 5;

[0042] Figure 17 Figure for cck-8 experiment result of comparative example 6;

[0043] Figure 18 Inhibition of CAP-induced TRPV1 expression by Example 1; **p<0.01 vs CAP;

[0044] Figure 19 Inhibition of CAP-induced TRPV1 expression by Example 2; **p<0.01 vs CAP;

[0045] Figure 20 Inhibition of CAP-induced TRPV1 expression by Example 3; **p<0.01 vs CAP;

[0046] Figure 21 Inhibition of CAP-induced TRPV1 expression by Example 4; **p<0.01 vs CAP;

[0047] Figure 22 Inhibition of CAP-induced TRPV1 expression by Example 5; **p<0.01 vs CAP;

[0048] Figure 23 Inhibition of CAP-induced TRPV1 expression by Example 6; **p<0.01 vs CAP;

[0049] Figure 24 Inhibition of CAP-induced TRPV1 expression by Example 7; **p<0.01 vs CAP;

[0050] Figure 25 Inhibition of CAP-induced TRPV1 expression by Example 8; **p<0.01 vs CAP;

[0051] Figure 26 Inhibition of CAP-induced TRPV1 expression by Example 9; **p<0.01 vs CAP;

[0052] Figure 27 Inhibition of CAP-induced TRPV1 expression by Example 10; **p<0.01 vs CAP;

[0053] Figure 28 Inhibition of CAP-induced TRPV1 expression for Example 11; **p<0.01 vs CAP;

[0054] Figure 29 Inhibition of CAP-induced TRPV1 expression for Comparative Example 1; **p<0.01 vs CAP;

[0055] Figure 30 Inhibition of CAP-induced TRPV1 expression for Comparative Example 2; **p<0.01 vs CAP;

[0056] Figure 31 Inhibition of CAP-induced TRPV1 expression for Comparative Example 3; **p<0.01 vs CAP;

[0057] Figure 32 Inhibition of CAP-induced TRPV1 expression for Comparative Example 4; **p<0.01 vs CAP;

[0058] Figure 33 Inhibition of CAP-induced TRPV1 expression for Comparative Example 5; **p<0.01 vs CAP;

[0059] Figure 34 Inhibition of CAP-induced TRPV1 expression for Comparative Example 6; *p<0.05, **p<0.01 vs CAP;

[0060] Figure 35 Elisa results for inhibition of CAP-induced IL-1a secretion for Example 1; **p<0.01 vs CAP;

[0061] Figure 36 Elisa results for inhibition of CAP-induced IL-1a secretion for Example 2; **p<0.01 vs CAP;

[0062] Figure 37 Elisa results for inhibition of CAP-induced IL-1a secretion for Example 3; **p<0.01 vs CAP;

[0063] Figure 38 Elisa results for inhibition of CAP-induced IL-1a secretion for Example 4; *p<0.05, **p<0.01 vs CAP;

[0064] Figure 39 Elisa results for inhibition of CAP-induced IL-1a secretion for Example 5; *p<0.05, **p<0.01 vs CAP;

[0065] Figure 40 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 6; **p<0.01 vs CAP;

[0066] Figure 41 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 7; **p<0.01 vs CAP;

[0067] Figure 42 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 8; **p<0.01 vs CAP;

[0068] Figure 43 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 9; **p<0.01 vs CAP;

[0069] Figure 44 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 10; **p<0.01 vs CAP;

[0070] Figure 45 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Example 11; **p<0.01 vs CAP;

[0071] Figure 46 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Comparative Example 1; **p<0.01 vs CAP;

[0072] Figure 47 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Comparative Example 2; **p<0.01 vs CAP;

[0073] Figure 48 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Comparative Example 3; **p<0.01 vs CAP;

[0074] Figure 49 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Comparative Example 4; **p<0.01 vs CAP;

[0075] Figure 50 Elisa assay results for inhibition of CAP-induced IL-1 alpha secretion for Comparative Example 5; *p<0.05, **p<0.01 vs CAP;

[0076] Figure 51For comparison of the results of the inhibition of CAP-induced IL-1a secretion Elisa test of Example 6; *p<0.05, **p<0.01 vs CAP. DETAILED DESCRIPTION

[0077] The application will be further described below in connection with specific embodiments. It should be understood that the following embodiments are only used to illustrate but not limit the scope of the application.

[0078] 1, Medicinal materials of the application

[0079] 1.1 Portulaca oleracea L. Portulaca oleracea Portulaca oleracea L., also known as Portulaca, Ants' cabbage, Wuxingcabbage, Longevity cabbage, Wuxing grass, etc., is an annual succulent herbaceous plant of the Portulacaceae Portulaca genus. Portulaca oleracea is a medicinal and edible plant, and its tender stems, leaves and flowers can be eaten as a healthy vegetable and a high-quality green medicinal feed. The whole grass and seeds of Portulaca oleracea can be used as medicinal materials, and have the effects of cooling blood and detoxifying, removing dampness and relieving stranguria, stopping dysentery, etc., and are often used to treat bacterial dysentery, sores, abscesses, tinea, eczema, etc.

[0080] From the 1960s to now, scholars at home and abroad have extracted various chemical components from Portulaca oleracea, mainly including organic acids, alkaloids, flavonoids, terpenes, polysaccharides, coumarins, steroids, anthocyanins, volatile oils, catecholamines, etc. Modern pharmacological studies have shown that Portulaca oleracea has good antibacterial, antioxidant, anti-aging, anti-allergic, immune-enhancing, etc. effects.

[0081] 1.2 Calendula officinalis L. Calendula officinalis Calendula officinalis L., also known as Calendula, Calendula, etc., is an annual herb of the Asteraceae Calendula genus. Its inflorescences can be used as medicine and have the effects of dry and cold, clearing the lungs and relieving cough, clearing heat and relieving asthma, etc., and are used to treat damp-heat or blood quality diseases, various inflammation and dark acne, etc. Its leaves can be used as salad, and the juice obtained by cold pressing the leaves can also be used to add fragrance to various foods such as soft drinks, ice foods, candies, baked foods. Calendula officinalis contains various active ingredients such as flavonoids, phenolic acids, sesquiterpenes, saponins, polysaccharides, etc. Modern studies have shown that Calendula officinalis has good antibacterial and antiviral, anti-inflammatory, antioxidant, anti-aging, moisturizing, anti-tumor, etc. effects.

[0082] 1.3 Scrophularia ningpoensis HEMSL (Hemsl.) HEMSL Scrophularia ningpoensis Hemsl.Scrophularia ningpoensis HEMSL, also named Yuan-shen, Beixuan-shen, Heishen, etc., is a plant of Scrophulariaceae. Its dried root can be used as medicine, which has the effects of clearing heat and cooling blood, nourishing yin and generating fluid, purging fire and detoxifying, softening and resolving. It is mainly used for treating heat entering the nutrient and blood, body fever and thirst, red tongue and spotty rash, bone dryness and cough, restlessness and insomnia, fluid deficiency and constipation, dry eyes and blurred vision, sore throat, scrofula, carbuncle and sore, etc. Scrophularia ningpoensis HEMSL mainly contains iridoid glycosides, phenylpropanoid glycosides, phytosterols, organic acids, flavonoids, triterpenoid saponins, volatile oils, sugars, alkaloids, and trace amounts of monoterpenes and diterpenes, etc. Modern research shows that Scrophularia ningpoensis HEMSL has good effects of protecting cardiovascular system, anti-tumor, anti-oxidation, anti-inflammatory, anti-bacterial, analgesic, etc. The Scrophularia ningpoensis HEMSL of the present application can also be selected from Scrophularia nodosa.

[0083] Example 1

[0084] 1, 100g of Calendula officinalis was added to 1750g of 0.2 mol / L sodium hydroxide solution and soaked for 16 hours;

[0085] 2, the soaking solution was extracted at 95-105 DEG C for 1 hour, and the residue was removed by gauze filtration;

[0086] 3, 1wt% of activated carbon was added to the filtrate, stirred at room temperature for 1 hour, and filtered until clear;

[0087] 4, the filtrate was continuously passed through anion and cation exchange resins, and the filtrate was obtained, concentrated to extract, dried, sterilized, and the capsaicin inhibitor, Calendula officinalis extract, was obtained.

[0088] Example 2

[0089] The difference between this example and Example 1 is that Calendula officinalis is replaced by Portulaca oleracea, and the capsaicin inhibitor obtained is Portulaca oleracea extract.

[0090] Example 3

[0091] The difference between this example and Example 1 is that Calendula officinalis is replaced by Scrophularia ningpoensis HEMSL, and the capsaicin inhibitor obtained is Scrophularia ningpoensis HEMSL extract.

[0092] Example 4

[0093] The difference between this example and Example 1 is that Calendula officinalis is replaced by Isatis indigotica Fort, and the capsaicin inhibitor obtained is Isatis indigotica Fort extract.

[0094] Example 5

[0095] The difference between this example and Example 1 is that Calendula officinalis is replaced by Lonicera japonica, and the capsaicin inhibitor obtained is Lonicera japonica extract.

[0096] Example 6

[0097] 1. 30 g of marigold and 70 g of Portulaca oleracea L. are added to 1500 g of 0.2 mol / L sodium hydroxide solution and soaked for 16 h;

[0098] 2. The soaking solution is extracted at 95-105°C for 1 h, and the residue is removed by gauze filtration;

[0099] 3. 1 wt% of activated carbon is added to the filtrate, stirred at room temperature for 1 h, and filtered until clear;

[0100] 4. The filtrate is further passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor.

[0101] Example 7

[0102] 1. 50 g of marigold and 50 g of Portulaca oleracea L. are added to 1500 g of 0.2 mol / L sodium hydroxide solution and soaked for 3 h;

[0103] 2. The soaking solution is extracted at 95-105°C for 1 h, and the residue is removed by gauze filtration;

[0104] 3. 1 wt% of activated carbon is added to the filtrate, stirred at room temperature for 1 h, and filtered until clear;

[0105] 4. The filtrate is further passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor.

[0106] Example 8

[0107] 1. 50 g of Portulaca oleracea L. and 50 g of Radix Aconiti are added to 1700 g of 0.5 mol / L arginine solution and soaked for 8 h;

[0108] 2. The soaking solution is extracted at 95-105°C for 2 h, and the residue is removed by gauze filtration;

[0109] 3. 1 wt% of activated carbon is added to the filtrate, stirred at room temperature for 1 h, and filtered until clear;

[0110] 4. The filtrate is further passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor.

[0111] Example 9

[0112] 1. 60 g of Portulaca oleracea L. and 40 g of Radix Aconiti are added to 1700 g of 0.5 mol / L arginine solution and soaked for 8 h;

[0113] 2. The soaking solution is extracted at 95-105°C for 2 h, and the residue is removed by gauze filtration;

[0114] 3. 1 wt% of activated carbon is added to the filtrate, stirred at room temperature for 1 h, and filtered until clear;

[0115] 4. The filtrate is continuously passed through anion and cation exchange resin, and the filtrate is collected, concentrated to extract, and dried to obtain the capsaicin inhibitor.

[0116] Example 10

[0117] 1. 40 g of Calendula and 60 g of Gastrodia were added to 1700 g of 0.5 mol / L potassium hydroxide solution and soaked for 2 h;

[0118] 2. The soaking solution was extracted at 95-105°C for 3 h, and the residue was removed by gauze filtration;

[0119] 3. Activated carbon was added to the filtrate in an amount of 1 wt%, and stirred at room temperature for 1 h, and filtered until clear;

[0120] 4. The filtrate was continuously passed through anion and cation exchange resin, and the filtrate was collected, concentrated to extract, and dried to obtain the capsaicin inhibitor.

[0121] Example 11

[0122] 1. 30 g of Calendula, 50 g of Spinach, and 20 g of Gastrodia were added to 1700 g of 0.5 mol / L arginine solution and soaked for 8 h;

[0123] 2. The soaking solution was extracted at 95-105°C for 2 h, and the residue was removed by gauze filtration;

[0124] 3. Activated carbon was added to the filtrate in an amount of 1 wt%, and stirred at room temperature for 1 h, and filtered until clear;

[0125] 4. The filtrate was continuously passed through anion and cation exchange resin, and the filtrate was collected, concentrated to extract, and dried to obtain the capsaicin inhibitor.

[0126] Comparative Example 1

[0127] 1. 60 g of Calendula and 40 g of Spinach were added to 1750 g of 0.5 mol / L arginine solution and soaked for 8 h;

[0128] 2. The soaking solution was extracted at 95-105°C for 2 h, and the residue was removed by gauze filtration;

[0129] 3. Activated carbon was added to the filtrate in an amount of 1 wt%, and stirred at room temperature for 1 h, and filtered until clear;

[0130] 4. The filtrate was continuously passed through anion and cation exchange resin, and the filtrate was collected, concentrated to extract, and dried to obtain the capsaicin inhibitor.

[0131] Comparative Example 2

[0132] 1. 25 g of Calendula and 75 g of Gastrodia were added to 1750 g of 0.5 mol / L arginine solution and soaked for 8 h;

[0133] 2. The soaking solution is extracted at 95-105°C for 2 hours, and the residue is removed by gauze filtration;

[0134] 3. 1 wt% activated carbon is added to the filtrate, and stirred at room temperature for 1 hour, and filtered until clear;

[0135] 4. The filtrate is continuously passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor.

[0136] Comparative Example 3

[0137] 1. 75 g of Portulaca oleracea and 25 g of Gastrodia elata are added to 1750 g of 0.5 mol / L arginine solution and soaked for 8 hours;

[0138] 2. The soaking solution is extracted at 95-105°C for 2 hours, and the residue is removed by gauze filtration;

[0139] 3. 1 wt% activated carbon is added to the filtrate, and stirred at room temperature for 1 hour, and filtered until clear;

[0140] 4. The filtrate is continuously passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor.

[0141] Comparative Example 4

[0142] 1. 100 g of Calendula officinalis is added to 1750 g of 50° ethanol and soaked for 16 hours;

[0143] 2. The soaking solution is extracted at 95-105°C for 1 hour, and the residue is removed by gauze filtration;

[0144] 3. 1 wt% activated carbon is added to the filtrate, and stirred at room temperature for 1 hour, and filtered until clear;

[0145] 4. The filtrate is continuously passed through anion and cation exchange resins, and the filtrate is taken, concentrated, and dried to obtain a capsaicin inhibitor: Calendula officinalis extract of Comparative Example.

[0146] Comparative Example 5

[0147] 1. 100 g of Portulaca oleracea is added to 1750 g of deionized water and soaked for 16 hours;

[0148] 2. The soaking solution is extracted at 95-105°C for 1 hour, and the residue is removed by gauze filtration;

[0149] 3. 1 wt% activated carbon is added to the filtrate, and stirred at room temperature for 1 hour, and filtered until clear;

[0150] 4. The filtrate continues to pass through anion and cation exchange resin, take the filtrate, concentrate to extract, dry, sterilize, and obtain the capsaicin inhibitor: Comparative Example Purslane Extract.

[0151] Comparative Example 6

[0152] 1. Scrophularia ningpoensis 100 g is soaked in 1750 g of 0.2 mol / L acetic acid solution for 16 h;

[0153] 2. The soaking solution is extracted at 95-105°C for 1 h, and the residue is removed by gauze filtration;

[0154] 3. Add 1 wt% of activated carbon to the filtrate, stir at room temperature for 1 h, and filter until clear;

[0155] 4. The filtrate continues to pass through anion and cation exchange resin, take the filtrate, concentrate to extract, dry, sterilize, and obtain the capsaicin inhibitor: Comparative Example Scrophularia ningpoensis Extract.

[0156] Table 1 is the composition and content of Examples 1-11 and Comparative Examples 1-6

[0157]

[0158] Note: The extraction temperature of the above examples and comparative examples is 95-105°C.

[0159] Scrophularia ningpoensis in Examples 3, 8-10, Comparative Example 1, and Comparative Example 6 is North Scrophularia ningpoensis; Scrophularia ningpoensis in Example 11 and Comparative Example 2 is forest Scrophularia ningpoensis.

[0160] Effect Example 1: Capsaicin stimulation model of human keratinocytes

[0161] 1. Experimental materials

[0162] Hacat cells (Chinese Academy of Sciences Cell Bank), capsaicin (MCE), capsaicinol (MCE), TRPV-1 primary antibody (cellsignaling technology), fluorescent secondary antibody (Bi Yun Tian), DAPI (Bi Yun Tian), IL-1α ELISA kit (Yun Klon), inverted fluorescence microscope (olympus), multifunctional enzyme marker (thermo fisher), etc.

[0163] Table 2: Preparation method of cell experiment test sample

[0164]

[0165] 1. Experimental method

[0166] 1.1 Cell toxicity test

[0167] Under sterile conditions, the test samples obtained in Table 1 were diluted with culture medium, and each test sample was uniformly diluted to: 0.005%, 0.01%, 0.02%, and 0.05%.

[0168] Hacat cells were cultured at a rate of 5 × 10 3 Cells were seeded into 96-well plates at a density of 100 cells / well and cultured in a 37°C, 5% CO2 incubator for 24 hours. When the cell density reached approximately 50%, the test sample was added. Twenty-four hours after addition, cell viability was assessed using the CCK-8 assay, and cell viability was calculated using the following formula.

[0169] Cell survival rate = (OD value of sample group - background OD value) / (OD value of blank control group - background OD value) × 100%

[0170] Note: Background OD value is not reflected in the data.

[0171] 1.2 Testing of the soothing efficacy of samples on human keratinocytes

[0172] According to the cytotoxicity test results, one concentration was selected as the soothing efficacy test concentration.

[0173] Hacat cells were cultured at a rate of 2 × 10 5 Cells were seeded at a density of 100 cells / well in a 6-well plate and cultured in a 37°C, 5% CO2 incubator for 24 hours before treatment. As shown in Table 3, cells were divided into a blank control (NC), a capsulitis induced group (CAP), a positive control (PC), and a sample group. The positive control and sample groups were treated with capsaicin at corresponding concentrations and incubated in a 37°C, 5% CO2 incubator for 4 hours. Capsaicin was added to the model, positive control, and sample groups and incubated in a 37°C, 5% CO2 incubator for 20 hours. At the end of the treatment period, the supernatant from each well was collected and assayed for IL-1α content using ELISA according to the kit instructions, and the inhibition rate was calculated. After cell fixation, TRPV1 protein expression was detected by immunofluorescence. Images were taken, and the mean fluorescence intensity of TRPV1 protein in the images was calculated using ImageJ software, and the inhibition rate was calculated.

[0174] Table 3 Overview of soothing efficacy experimental groups

[0175]

[0176] Inhibition rate % = (1-expression level of sample group / expression level of CAP-induced group) × 100%

[0177] 1.3 Calculation of Combination Index (CI)

[0178] Combination Index (CI) is a method to evaluate the drug combination effect, which was proposed by Chou and Talalay in 1984. The method is based on the dose-effect curve of drugs, and the ratio of actual effect and theoretical effect of combination is calculated to determine whether the combination has synergistic effect, additive effect or antagonistic effect. CI value less than 0.9 indicates synergistic effect, the smaller the value, the stronger the synergistic effect; CI value between 0.9 and 1.1 indicates additive effect; CI value greater than 1.1 indicates antagonistic effect, the greater the value, the stronger the antagonistic effect.

[0179] The CI value was obtained by analyzing the calculated inhibition rate using CompuSyn software.

[0180] 1.4 Statistical analysis of experimental data

[0181] All data were expressed as mean ± standard deviation, and one-way ANOVA was used for comparison between groups. P<0.05 was considered to have significant difference, and P<0.01 was considered to have extremely significant difference.

[0182] 1.5 Experimental results

[0183] 1.5.1 Cell toxicity detection results

[0184] Table 4: CCK-8 experimental results of Example 1 - Calendula extract

[0185]

[0186] Table 5: CCK-8 experimental results of Example 2 - Purslane extract

[0187]

[0188] Table 6: CCK-8 experimental results of Example 3 - Scrophularia extract

[0189]

[0190] Table 7: CCK-8 experimental results of Example 4 - Isatis root extract

[0191]

[0192] Table 8: CCK-8 experimental results of Example 5 - Honeysuckle flower extract

[0193]

[0194] Table 9: CCK-8 experimental results of Example 6

[0195]

[0196] Table 10 Example 7 cck-8 experimental results

[0197]

[0198] Table 11 Example 8 cck-8 experimental results

[0199]

[0200] Table 12 Example 9 cck-8 experimental results

[0201]

[0202] Table 13 Example 10 cck-8 experimental results

[0203]

[0204] Table 14 Example 11 cck-8 experimental results

[0205]

[0206] Table 15 Comparative Example 1 cck-8 experimental results

[0207]

[0208] Table 16 Comparative Example 2 cck-8 experimental results

[0209]

[0210] Table 17 Comparative Example 3 cck-8 experimental results

[0211]

[0212] Table 18 Comparative Example 4 cck-8 experimental results

[0213]

[0214] Table 19 Comparative Example 5 cck-8 experimental results

[0215]

[0216] Table 20 Comparative Example 6 cck-8 experimental results

[0217]

[0218] Result analysis: According to the cck-8 toxicity experiment results, 0.005-0.02% concentration was selected for subsequent experiments.

[0219] 2.4.2 Soothing efficacy test

[0220] 2.4.2.1 TRPV-1 protein expression

[0221] Table 21 Example 1 - Calendula extract inhibits CAP-induced TRPV1 expression

[0222]

[0223] Result analysis: As shown in the results, the extract of Calendula officinalis at a concentration of 0.005-0.02% can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 32.67%±4.90%, 39.69%±3.04%, and 44.49%±4.76%, respectively.

[0224] Table 22 Example 2 - Portulaca oleracea inhibits CAP-induced TRPV1 expression

[0225]

[0226] Result analysis: As shown in the results, the purslane extract at a concentration of 0.005-0.02% can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 34.27%±4.19%, 39.71%±4.24%, and 46.54%±4.06%, respectively.

[0227] Table 23 Example 3 - Scrophulariaceae extract inhibits CAP-induced TRPV1 expression

[0228]

[0229] Result analysis: As shown in the results, Scrophularia ningpoensis extract at a concentration of 0.005-0.02% can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 39.80%±0.72%, 46.79%±0.75%, and 53.46%±0.13%, respectively.

[0230] Table 24 Example 4 - Isatis indigotica root extract inhibits CAP-induced TRPV1 expression

[0231]

[0232] Results analysis: As shown in the results, the radix isatidis extract can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at 0.01-0.02% concentration (p<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 9.92%±1.67%, 12.71%±3.28% respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 9.92%±1.67%, 12.71%±3.28% respectively.

[0233] Table 25 Example 5 - Inhibition of TRPV1 expression induced by CAP by honeysuckle flower extract

[0234]

[0235] Results analysis: As shown in the results, the honeysuckle flower extract can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at 0.01-0.02% concentration (p<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 11.74%±1.35%, 16.93%±1.50% respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 11.74%±1.35%, 16.93%±1.50% respectively.

[0236] Table 26 Example 6 - Inhibition of TRPV1 expression induced by CAP

[0237]

[0238] Results analysis: As shown in the results, Example 6 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at 0.005-0.02% concentration (p<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 34.14%±0.65%, 39.44%±0.24%, 49.98%±3.68% respectively.

[0239] Table 27 Example 7 - Inhibition of TRPV1 expression induced by CAP

[0240]

[0241] Results analysis: As shown in the results, Example 7 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at 0.005-0.02% concentration (p<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 39.38%±1.99%, 41.44%±2.82%, 49.79%±1.43% respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 39.38%±1.99%, 41.44%±2.82%, 49.79%±1.43% respectively.

[0242] Table 28 Example 8 - Inhibition of TRPV1 expression induced by CAP

[0243]

[0244] Results analysis: As shown in the results, Example 8 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 45.44%±0.92%, 51.49%±1.06%, 59.63%±1.10%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 45.44%±0.92%, 51.49%±1.06%, 59.63%±1.10%, respectively.

[0245] Table 29 Example 9 inhibits the expression of CAP-induced TRPV1

[0246]

[0247] Results analysis: As shown in the results, Example 9 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 44.21%±1.11%, 50.79%±0.62%, 57.97%±0.96%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 44.21%±1.11%, 50.79%±0.62%, 57.97%±0.96%, respectively.

[0248] Table 30 Example 10 inhibits the expression of CAP-induced TRPV1

[0249]

[0250] Results analysis: As shown in the results, Example 10 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 41.39%±0.89%, 47.86%±0.23%, 55.82%±0.23%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 41.39%±0.89%, 47.86%±0.23%, 55.82%±0.23%, respectively.

[0251] Table 31 Example 11 inhibits the expression of CAP-induced TRPV1

[0252]

[0253] Results analysis: As shown in the results, Example 11 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are: 41.39%±0.89%, 47.86%±0.23%, 55.82%±0.23%, respectively. ** p<0.01 vs CAP) and has a dose-effect relationship; the inhibition rates are 45.64%±3.13%, 52.63%±2.16%, 60.23%±1.29% respectively.

[0254] Table 32 Inhibition of CAP-induced expression of TRPV1 by Comparative Example 1

[0255]

[0256] Result analysis: As shown in the results, Example 5 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 45.64%±3.13%, 52.63%±2.16%, 60.23%±1.29% respectively. ** p <0.01 vs CAP) and has a dose-effect relationship; the inhibition rates are 45.64%±3.13%, 52.63%±2.16%, 60.23%±1.29% respectively.

[0257] Table 33 Inhibition of CAP-induced expression of TRPV1 by Comparative Example 2

[0258]

[0259] Result analysis: As shown in the results, Comparative Example 1 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 38.38%±2.70%, 44.04%±4.52%, 52.93%±1.03% respectively. ** p <0.01 vs CAP) and has a dose-effect relationship; the inhibition rates are 45.64%±3.13%, 52.63%±2.16%, 60.23%±1.29% respectively.

[0260] Table 34 Inhibition of CAP-induced expression of TRPV1 by Comparative Example 3

[0261]

[0262] Result analysis: As shown in the results, Comparative Example 3 can significantly inhibit the expression of TRPV1 of Hacat cells induced by capsaicin at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 37.53%±3.27%, 41.26%±2.69%, 50.40%±2.85% respectively. ** p <0.01 vs CAP) and has a dose-effect relationship; the inhibition rates are 45.64%±3.13%, 52.63%±2.16%, 60.23%±1.29% respectively.

[0263] Table 35 Inhibition of CAP-induced expression of TRPV1 by Comparative Example 4

[0264]

[0265] Result analysis: As shown in the results, comparative example 4 can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin at a concentration of 0.01-0.02% ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were: 11.09%±2.50% and 17.67%±1.30%, respectively.

[0266] Table 36 Comparative Example 5 inhibits CAP-induced TRPV1 expression

[0267]

[0268] Result analysis: As shown in the results, comparative example 5 can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin at a concentration of 0.01-0.02% ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were: 10.49%±2.04% and 16.76%±1.36%, respectively.

[0269] Table 37 Comparative Example 6 inhibits CAP-induced TRPV1 expression

[0270]

[0271] Result analysis: As shown in the results, comparative example 6 can significantly inhibit the expression of TRPV1 in Hacat cells induced by capsaicin at a concentration of 0.01-0.02% ( * p <0.05, ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 7.38%±2.46% and 14.86%±1.97%, respectively.

[0272] Table 38 Inhibition rate and CI value of samples on CAP-induced TRPV1 expression

[0273]

[0274] Analysis of results: As shown in the results, the inhibition rates of the combination of two samples and the combination of three samples on capsaicin-induced TRPV1 expression were higher than those of the single samples, and the CI values ​​were between 0.3 and 0.8, indicating that there was a synergistic effect between the samples; the cosmetic capsaicin irritation inhibitors prepared using the process of Comparative Examples 4-6 were significantly less effective than the cosmetic capsaicin irritation inhibitors of Examples 1-3.

[0275] 2.4.2.2 IL-1α secretion

[0276] Table 39 Example 1 - Calendula extract inhibits CAP-induced IL-1a secretion

[0277]

[0278] Results analysis: As shown in the results, the Calendula extract at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1a by Hacat cells induced by capsaicin (P < 0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 18.69% ± 1.41%, 34.65% ± 0.31%, and 42.96% ± 0.90%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 18.69% ± 1.41%, 34.65% ± 0.31%, and 42.96% ± 0.90%, respectively.

[0279] Table 40 Example 2 - Portulaca extract inhibits CAP-induced IL-1a secretion

[0280]

[0281] Results analysis: As shown in the results, the Portulaca extract at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1a by Hacat cells induced by capsaicin (P < 0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 19.54% ± 1.38%, 35.86% ± 1.50%, and 43.55% ± 2.25%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 19.54% ± 1.38%, 35.86% ± 1.50%, and 43.55% ± 2.25%, respectively.

[0282] Table 41 Example 3 - Extract of Scrophularia inhibits CAP-induced IL-1a secretion

[0283]

[0284] Results analysis: As shown in the results, the Scrophularia extract at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1a by Hacat cells induced by capsaicin (P < 0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 28.56% ± 0.62%, 40.38% ± 2.05%, and 47.67% ± 0.68%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 28.56% ± 0.62%, 40.38% ± 2.05%, and 47.67% ± 0.68%, respectively.

[0285] Table 42 Example 4 - Extract of Isatis root inhibits CAP-induced IL-1a secretion

[0286]

[0287] Results analysis: As shown in the results, the Isatis root extract of Example 4 at a concentration of 0.01-0.02% can inhibit the secretion of IL-1a by Hacat cells induced by capsaicin (P < 0.01 vs CAP), and has a dose-effect relationship; the inhibition rates were 19.54% ± 1.38%, 35.86% ± 1.50%, and 43.55% ± 2.25%, respectively. *p <0.05, ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 9.12%±0.13% and 15.40%±3.67%, respectively.

[0288] Table 43 Example 5 - Honeysuckle extract inhibits CAP-induced IL-1α secretion

[0289]

[0290] Result analysis: As shown in the results, the honeysuckle extract of Example 5 at a concentration of 0.02% can inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( * p <0.05 vs CAP); inhibition rate: 15.93%±0.66%.

[0291] Table 44 Example 6 inhibits CAP-induced IL-1α secretion

[0292]

[0293] Result analysis: As shown in the results, Example 6 at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 33.74%±3.76%, 44.05%±1.30%, and 54.00%±0.88%, respectively.

[0294] Table 45 Example 7 Inhibition of CAP-induced IL-1α secretion

[0295]

[0296] Result analysis: As shown in the results, Example 7 at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 31.37%±1.75%, 43.54%±1.95%, and 52.84%±0.12%, respectively.

[0297] Table 46 Example 8 Inhibition of CAP-induced IL-1α secretion

[0298]

[0299] Result analysis: As shown in the results, Example 8 at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 36.57%±1.72%, 47.40%±4.00%, and 59.38%±3.99%, respectively.

[0300] Table 47 Example 9 inhibits CAP-induced IL-1α secretion

[0301]

[0302] Result analysis: As shown in the results, Example 9 at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 36.22%±2.55%, 46.50%±0.49%, and 58.46%±1.43%, respectively.

[0303] Table 48 Example 10 Inhibits CAP-induced IL-1α secretion

[0304]

[0305] Result analysis: As shown in the results, Example 10 at a concentration of 0.005-0.02% can significantly inhibit the secretion of IL-1α by Hacat cells induced by capsaicin ( ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 36.01%±7.06%, 45.52%±4.12%, and 57.78%±5.25%, respectively.

[0306] Table 49 Example 11 Inhibition of CAP-induced IL-1α secretion

[0307]

[0308] Result analysis: As shown in the results, Example 11 can inhibit the secretion of IL-1α by Hacat cells induced by capsaicin at a concentration of 0.005-0.02%. ** p <0.01 vs CAP), and there was a dose-effect relationship; the inhibition rates were 38.38%±3.03%, 48.46%±4.98%, and 60.12%±3.23%, respectively.

[0309] Table 50 Comparative Example 1 inhibits CAP-induced IL-1α secretion

[0310]

[0311] Result analysis: As shown in the results, comparative example 1 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 22.85%±2.47%, 37.82%±3.51%, and 45.65%±3.39%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 22.85%±2.47%, 37.82%±3.51%, and 45.65%±3.39%, respectively.

[0312] Table 51 Inhibition of CAP-induced IL-1α secretion by comparative example 2

[0313]

[0314] Result analysis: As shown in the results, comparative example 2 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 24.65%±4.13%, 39.53%±0.51%, and 47.07%±4.26%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 22.85%±2.47%, 37.82%±3.51%, and 45.65%±3.39%, respectively.

[0315] Table 52 Inhibition of CAP-induced IL-1α secretion by comparative example 3

[0316]

[0317] Result analysis: As shown in the results, comparative example 3 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.005-0.02% (P<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 24.80%±7.82%, 39.67%±3.11%, and 46.65%±3.14%, respectively. ** p <0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 22.85%±2.47%, 37.82%±3.51%, and 45.65%±3.39%, respectively.

[0318] Table 53 Inhibition of CAP-induced IL-1α secretion by comparative example 4

[0319]

[0320] Result analysis: As shown in the results, comparative example 4 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.02% (P<0.01 vs CAP); the inhibition rate is 17.18%±2.92%. ** p <0.01 vs CAP; the inhibition rate is 17.18%±2.92%.

[0321] Table 54 Inhibition of CAP-induced IL-1α secretion by Comparative Example 5

[0322]

[0323] Result analysis: As shown in the results, Comparative Example 5 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.02% (p<0.05 vs CAP), and the inhibition rate is 11.33%±3.87%. * p <0.05 vs CAP); the inhibition rate was 11.33%±3.87%.

[0324] Table 55 Inhibition of CAP-induced IL-1α secretion by Comparative Example 6

[0325]

[0326] Result analysis: As shown in the results, Comparative Example 6 can inhibit the secretion of IL-1α induced by capsaicin in Hacat cells at a concentration of 0.01-0.02% (p<0.05, **p<0.01 vs CAP), and has a dose-effect relationship; the inhibition rates are 9.65%±3.73%, 14.50%±2.52%, respectively.

[0327] Table 56 Inhibition rate of CAP-induced IL-1α secretion and CI value of samples

[0328]

[0329] Result analysis: As shown in the results, the inhibition rate of the combination of two samples, the combination of three samples on the secretion of IL-1α induced by capsaicin is higher than that of single action, and the CI value is between 0.4-0.7, indicating that there is a synergistic effect between the samples; the effect of the cosmetic capsaicin stimulant inhibitor prepared by the process of Comparative Examples 4-6 is obviously insufficient compared with the effect of Examples 1-3.

[0330] In summary, the cosmetic capsaicin stimulant inhibitor provided by the present application can effectively inhibit the expression of TRPV1 and the secretion of IL-1α.

[0331] The specific embodiments of the present application are described in detail above, but they are only examples, and the present application is not limited to the specific embodiments described above. Any equivalent modifications and alternatives to the present application made by those skilled in the art are also within the scope of the present application. Therefore, equivalent transformations and modifications made without departing from the spirit and scope of the present application should be included in the scope of the present application.

Claims

1. A method for producing a cosmetic capsaicin stimulant inhibitor, characterized by, It comprises the following steps: A. Soaking medicinal materials with 15-20 times weight of extraction solvent for 2-16 hours to obtain soaking liquid; the extraction solvent is 0.2-0.8 mol / L aqueous alkali solution; B. Extracting the soaking liquid at 95-105℃ for 1-3 hours; Wherein, the medicinal materials are Gynura japonica and Herba Portulacae, and the weight ratio of Gynura japonica and Herba Portulacae is 30-50:50-70; or, The medicinal materials are Gynura japonica and Scrophularia ningpoensis, and the weight ratio of Gynura japonica and Scrophularia ningpoensis is 40:60; or, The medicinal materials are Herba Portulacae and Scrophularia ningpoensis, and the weight ratio of Herba Portulacae and Scrophularia ningpoensis is 50-60:40-50; or, The medicinal materials are Gynura japonica, Herba Portulacae and Scrophularia ningpoensis, and the weight ratio of Gynura japonica, Herba Portulacae and Scrophularia ningpoensis is 30:50:

20.

2. The method for preparing a cosmetic capsaicin stimulants inhibitor according to claim 1, characterized by, After step B, it further comprises the following steps: C. Removing filter residue, decolorizing, filtering, desalting to prepare cosmetic capsaicin stimulation inhibitor.

3. The method for preparing a cosmetic capsaicin stimulants inhibitor according to claim 1, wherein the capsaicin stimulants inhibitor is prepared by adding the capsaicin stimulants inhibitor to the cosmetic composition. The concentration of the aqueous alkali solution is 0.2-0.5 mol / L.

4. The method for preparing a cosmetic capsaicin stimulants inhibitor according to claim 1, wherein The aqueous alkali solution in step A is one or more combinations of sodium hydroxide aqueous solution, potassium hydroxide aqueous solution, sodium carbonate aqueous solution and arginine aqueous solution.

5. A cosmetic capsaicin stimulation inhibitor prepared by the preparation method of the cosmetic capsaicin stimulation inhibitor according to any one of claims 1-4.

6. Use of the cosmetic capsaicin stimulation inhibitor according to claim 5 in the preparation of skin external preparation with soothing effect.

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