动物造模,银屑病 z-bio 2021-12-31 513

　　Objective This study intends to use the imiquimod (IMQ) mouse psoriasis model to explore the regulation of Cosentyx (Cosentyx) on skin inflammation and autophagy in psoriasis mice through the C5a / C5aR1 pathway.

　　Methods 27 8-week-old male BALB/c mice were randomly divided into 3 groups (9 mice in each group): Blank group, Model group, and Cosentyx treatment group. treat group), except for the blank control group, the other two groups used imiquimod (IMQ) to prepare psoriasis models. Twice, 4.5 mg/kg each time) intervention. The effect of Keshan Ting on the pathological damage of the skin tissue of psoriasis model mice was observed by HE staining, and the levels of pro-inflammatory factors IL-4, IL-8, TNF-α, and IL-1β in mouse skin lesions were detected by ELISA. Secretion, detect myeloperoxidase (MPO) activity in mouse skin lesions by spectrophotometry, and detect Beclin 1 expression and LC3-Ⅱ/LC3-I value in mouse skin lesions by Western blot. Immunohistochemical method was used to detect the expression levels of C5a, C3, C5aR1, C1qB in mouse skin lesions.

　　As a result, it can inhibit the expression of IL-4, IL-8, TNF-α, IL-1β and MPO in the skin lesions, and increase the expression of Beclin 1 and the LC3-Ⅱ/LC3-I ratio. Down-regulated the expression of C1qB, C3, C5a, and C5aR1 molecules in the C5a / C5aR1 pathway.

　　Conclusion Keshanting inhibits the C5a / C5aR1 pathway, and can regulate the expression of inflammatory factors in psoriasis skin lesions through the C5a / C5aR1 pathway, slowing down the inflammatory response of psoriasis, and at the same time, it can enhance the psoriatic skin lesions. Autophagy, but it is unclear whether the C5a / C5aR1 pathway regulates autophagy in psoriasis skin lesions, so the mechanism needs to be further determined.