动物造模,银屑病 z-bio 2022-09-28 328

　　Objective To investigate the regulatory effect of Cosentyx on skin inflammation and autophagy in psoriatic mice through the C5a/C5aR1 pathway through the imiquimod (IMQ) mouse model of psoriasis.

　　Methods Twenty-seven 8-week-old male BALB/c mice were randomly divided into 3 groups (nine mice in each group): blank control group (Blank group), psoriasis model group (Model group), and Cosentyx-treated group (Cosentyx- treat group), except for the blank control group, the other two groups were treated with imiquimod (IMQ) to prepare psoriasis models, and the cosentine treatment group was given subcutaneous injection of cosentine (on days 1, 6, and 13, 1 d). twice, 4.5 mg/kg each time) intervention. HE staining was used to observe the effect of Corsentine on the pathological damage of skin tissue of psoriasis model mice, and ELISA was used to detect the pro-inflammatory factors IL-4, IL-8, TNF-α and IL-1β in mouse skin lesions. The secretion of mouse skin lesions was detected by spectrophotometry, and the activity of myeloperoxidase (MPO) in mouse skin lesions was detected by Western blotting. The expression levels of C5a, C3, C5aR1 and C1qB in mouse skin lesions were detected by immunohistochemistry.

　　Results Kesenting inhibited the expression of IL-4, IL-8, TNF-α, IL-1β and MPO in skin lesions, and increased the expression of Beclin 1 and the ratio of LC3-II/LC3-I. Downregulated the expression of C1qB, C3, C5a, C5aR1 molecules in the C5a/C5aR1 pathway.

　　Conclusion Corsentine inhibits the C5a/C5aR1 pathway, can regulate the expression of inflammatory factors in psoriatic skin lesions through the C5a/C5aR1 pathway, and slow down the inflammatory response of psoriasis. Autophagy, but it is impossible to determine whether Cosentyx regulates autophagy in psoriatic skin lesions through the C5a/C5aR1 pathway, so the mechanism needs to be further determined.