Use of tetrahydropalmatine in preparation of drug for treating atopic dermatitis

Abstract

A use of tetrahydropalmatine in the preparation of a drug for treating atopic dermatitis. The treatment of atopic dermatitis with tetrahydropalmatine is researched. The research shows that tetrahydropalmatine can significantly improve atopic dermatitis caused by calcipotriol and inhibit skin epidermal barrier damage, pruritus factor release and inflammatory factor release caused by tetrahydropalmatine, so that tetrahydropalmatine can be used for the treatment of atopic dermatitis.

Description

Application of tetrahydropalmatine in preparing medicine for treating atopic dermatitis Technical Field

[0001] The invention belongs to the field of preparation of anti-atopic dermatitis drugs and relates to the application of tetrahydropalmatine in the preparation of drugs for treating atopic dermatitis. Background Art

[0002] Modern pharmacological research has revealed that the main pharmacological component of Corydalis yanhusuo is tetrahydropalmatine, also known as tetrahydropalmatine and tetrahydrotetrahydropalmatine. Tetrahydropalmatine has a weaker analgesic effect than pethidine and morphine, but is less addictive and more potent than common antipyretic analgesics. It can induce hypotension and bradycardia in rats by antagonizing striatal dopamine D2 receptors. It has significant therapeutic effects on pain caused by the gastrointestinal and hepatobiliary systems, and can also relieve labor pains, headaches, and concussion headaches. It is also used to alleviate mental stress such as irritability and anxiety, and to treat insomnia caused by neurasthenia.

[0003] Atopic dermatitis is a chronic skin disease that is prone to relapse. Its main clinical manifestation is recurrent chronic eczema-like rash, accompanied by significant skin dryness and itching.

[0004] Currently, the drugs commonly used to treat atopic dermatitis are glucocorticoids and antibiotics. However, these drugs can only alleviate the symptoms of atopic dermatitis and have significant adverse reactions in the human body, making them unsuitable for long-term use. Therefore, there is currently no drug that can completely cure atopic dermatitis, and the development of new, safe and effective drugs for the treatment of atopic dermatitis is urgently needed.

[0005] Currently, there are no reports on the application of tetrahydropalmatine as an anti-specific dermatitis drug. Technical issues

[0006] In order to overcome the shortcomings of the prior art, the present invention aims to provide a method for preparing a drug for treating atopic dermatitis. Technical Solutions

[0007] Application of tetrahydropalmatine in the preparation of medicines for treating atopic dermatitis.

[0008] Preferably, the drug is a drug that inhibits the production of skin scales.

[0009] Preferably, the drug is a drug that inhibits the release of skin itching mediators.

[0010] Preferably, the drug is a drug that inhibits damage to the skin epidermal barrier.

[0011] Preferably, the drug is a drug that inhibits the release of inflammatory factors in the skin epidermis.

[0012] A medicine for treating atopic dermatitis, comprising tetrahydropalmatine.

[0013] Preferably, the dosage form of the drug is a gel, ointment, cream, powder, aqueous solution or lotion.

[0014] Furthermore, the concentration of tetrahydropalmatine in the drug is 0.1-0.4 g / mL. Beneficial effects

[0015] The present invention studies the use of tetrahydropalmatine in the treatment of atopic dermatitis. The studies show that tetrahydropalmatine can significantly improve the symptoms of atopic dermatitis caused by calcipotriol, inhibit the damage to the skin epidermal barrier, the release of itching factors and the release of inflammatory factors caused by tetrahydropalmatine, and confirm that tetrahydropalmatine can be used to treat atopic dermatitis. BRIEF DESCRIPTION OF THE DRAWINGS

[0016] FIG1 is a graph showing the results of the inhibition of tetrahydropalmatine on calcipotriol-induced epidermal barrier damage in mouse skin;

[0017] FIG2 is a graph showing the results of the inhibition of tetrahydropalmatine on calcipotriol-induced weight loss in mice;

[0018] FIG3 is a graph showing the results of the inhibition of tetrahydropalmatine on the number of scratching times induced by calcipotriol in mice;

[0019] FIG4 shows the results of the inhibition of tetrahydropalmatine on the increase in ear thickness of mice induced by calcipotriol. Modes for Carrying Out the Invention

[0020] In order to enable those skilled in the art to better understand the solutions of the present invention, the technical solutions in the embodiments of the present invention will be clearly and completely described below in conjunction with the drawings in the embodiments of the present invention. Obviously, the embodiments described are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without making creative efforts should fall within the scope of protection of the present invention.

[0021] Example 1 Preparation of Tetrahydropalmatine Gel

[0022] Take 6.67 g of 30% poloxamer P407, 1 g of 45% poloxamer P188, and 2.33 g of H2O and mix them evenly to prepare a gel matrix. Then, tetrahydropalmatine and the gel matrix are mixed in a mass ratio of 1:9 to prepare a tetrahydropalmatine gel with a crude drug amount of 0.25 g / mL. Centrifuge at 5000 r for 5 minutes to obtain tetrahydropalmatine gel.

[0023] The tetrahydropalmatine of the present invention can also be prepared into ointment, cream, powder, aqueous solution or lotion.

[0024] Example 2 Tetrahydropalmatine inhibits calcipotriol-induced atopic dermatitis symptoms in mice

[0025] 1. Experimental Materials

[0026] Tetrahydropalmatine, calcipotriol (purchased from MCE), 6-8 week old female C57 mice (purchased from the Experimental Animal Center of Xi'an Jiaotong University)

[0027] 2. Experimental methods

[0028] This study used calcipotriol (MC903) to establish an atopic dermatitis model. First, mice were divided into the NC group (blank control), the Vehicle group (negative control), the positive drug group (glucocorticoid group), and the tetrahydropalmatine group. Mice in the NC group received no treatment and were housed normally. Mice in the other groups were treated with a calcipotriol ethanol solution applied to their ears, with 20 μL applied bilaterally to each ear for 13 consecutive days, to establish an atopic dermatitis model. Mice in the Vehicle group received no other medications except for the 13th day. Mice in the positive drug group received a glucocorticoid application daily to their ears starting on day 8, while mice in the tetrahydropalmatine group received a gel-based application of tetrahydropalmatine (0.25 g / mL) daily to their ears starting on day 8. On day 13, the number of ear scratches (within 10 minutes) and the presence of scales were counted for each group. Mice were sacrificed, and ear tissue was collected for examination.

[0029] 3. Experimental results

[0030] As shown in Figure 1, the ear skin of mice in the NC group showed no significant changes, while the ears of mice in the Vehicle group, which received calcipotriol, showed increased scales and a damaged epidermal barrier. This is due to calcipotriol-induced atopic dermatitis in the ears of mice, which caused itching and constant scratching. When corydalis gel was applied to the ears of mice with atopic dermatitis symptoms, the ears showed less scales and less damage to the epidermal barrier than those in the Vehicle group, indicating that corydalis can effectively inhibit the damage to the epidermal barrier caused by calcipotriol-induced scratching. When the ears of mice were applied with the positive drug glucocorticoid, although the damage to the epidermal barrier was also reduced, wrinkling of the ears was observed, indicating that the positive drug caused an adverse reaction in the mice. However, the mice in the corydalis group did not show any wrinkling, indicating that corydalis did not cause any adverse reactions in the mice, indicating that corydalis is non-toxic.

[0031] As shown in Figure 2, the weight of mice in the NC group showed an overall upward trend, while the weight of mice in the Vehicle group, which received calcipotriol, decreased significantly. The weight of mice treated with tetrahydropalmatine was comparable to that of the Vehicle group, while the weight loss of mice treated with the positive drug was accelerated. This indicates that the positive drug glucocorticoid exacerbated the weight loss of mice, indicating that the positive drug glucocorticoid has a certain degree of toxicity to mice, while the Corydalis extract is not toxic to mice.

[0032] As shown in Figure 3, mice in the NC group scratched their ears less frequently, while mice in the Vehicle group, which received calcipotriol, scratched their ears more frequently, indicating that calcipotriol causes an increase in the levels of itch mediators in the skin. Furthermore, mice in the Tetrahydropalmatine group scratched their ears significantly less frequently than those in the Vehicle group, indicating that Tetrahydropalmatine can effectively inhibit the increase in itch mediator levels in the skin caused by calcipotriol.

[0033] As shown in Figure 4, compared to the ear thickness of the NC group, the ear thickness of the mice in the Vehicle group treated with calcipotriol increased, indicating that calcipotriol caused an increase in the levels of inflammatory factors in the skin epidermis. The ear thickness of the mice treated with tetrahydropalmatine was significantly reduced compared to the Vehicle group, indicating that tetrahydropalmatine can effectively inhibit the increase in the levels of inflammatory factors in the skin epidermis.

[0034] As shown in Figures 1-4, applying calcipotriol to the ears of mice resulted in significant atopic dermatitis symptoms, including increased scratching, weight loss, damage to the epidermal barrier, and elevated levels of inflammatory factors in the skin. Applying tetrahydropalmatine to the ears of mice effectively inhibited damage to the epidermal barrier, the release of itch mediators, and the release of inflammatory factors in the skin, alleviating atopic dermatitis symptoms and reducing scratching. Tetrahydropalmatine significantly improved atopic dermatitis symptoms in mice and was less toxic than commonly used glucocorticoids in clinical practice.

[0035] The technical idea of ​​the present invention is to illustrate the technical idea of ​​the present invention, and the protection scope of the present invention cannot be limited by this. Any changes made on the basis of the technical solution in accordance with the technical idea proposed by the present invention shall fall within the protection scope of the claims of the present invention.

Claims

1. Application of chlorhexidine in the preparation of drugs for the treatment of atopic dermatitis.

2. The use according to claim 1, characterized in that The medicine is a medicine for inhibiting the production of skin squama.

3. The use according to claim 1, characterized in that The medicine is a medicine for inhibiting the release of skin itching mediators.

4. The use according to claim 1, characterized in that The medicine is a medicine for inhibiting damage to the skin epidermal barrier.

5. The use according to claim 1, characterized in that The medicine is a medicine for inhibiting the release of skin epidermal inflammatory factors.

6. A drug for treating atopic dermatitis, characterized in that: The drug contains tetrahydropalmatine.

7. The drug for treating atopic dermatitis according to claim 6, characterized in that: The dosage form of the medicine is gel, ointment, cream, powder, aqueous solution or lotion.

8. The drug for treating atopic dermatitis according to claim 7, characterized in that: The concentration of tetrahydropalmatine in the drug is 0.1-0.4 g / mL.

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