动物实验,免疫性脑脊髓炎 z-bo 2020-08-27 485

　　Objective: To explore the role of inducible intestinal peptide (VIP) that regulates the balance of CD4 + CD25 + Treg/Th17 in the prevention and treatment of experimental autoimmune encephalomyelitis (EAE).

　　Method: 60 healthy Wistar female rats were randomly divided into normal control group, EAE control group, VIP low-dose control group and VIP high-dose control group. The EAE model is induced by myelin basic protein (MBP) + complete Freund's adjuvant (CFA). From the day of modeling, VIP 4mol/kg (0.2 mL) and 16mol/kg (0.8 mL) were intraperitoneally injected every other day to VIP low-dose and high-dose prevention groups. The normal control group and the EAE control group were injected with 0.8 mL of saline for 10 consecutive days. Observe the incidence of rats; observe the basic pathological changes of brain tissue by HE staining; detect the percentage of CD4 + CD25 + Treg and Th17 cells in spleen tissue by flow cytometry; detect TGF-β1 and IL-17A in E. coli by brain tissue ELISA Changes in factor content.

　　Results: Compared with the EAE control group, the rats treated with VIP had a longer seizure latency, shorter progression and reduced peak seizure neurological dysfunction score (NDS). HE staining did not show normal control brain tissue. The degree of inflammatory cell infiltration in the brain tissue of the VIP treatment group was significantly lower than that of the EAE group; the proportion of CD4 + CD25 + Treg cell subsets in the spleen tissue of the VIP group was higher than that of the EAE control group, while the proportion of Th17 cell subsets decreased. There is a specific dose-effect relationship. The content of TGF-β1 in the brain tissue of VIP group was significantly higher than that of EAE group and IL-17A content was significantly lower than that of EAE group. There is a specific dose dependence between each group.

　　Conclusion: VIP up-regulates the proportion of CD4 + CD25 + Treg cells, down-regulates the proportion of Th17 cells, and inhibits the expression of TGF-β1 factor by inhibiting the expression of IL-17A factor. It promotes, thereby reducing the infiltration of inflammatory cells in the brain tissue, and plays a role in the prevention and treatment of EAE.