摘要:
Objective: To investigate the Effect of saikosaponin A on Treg and Th17 immune balance in depressive rats. Methods: The rat depression model was established with reference to the Katz method, and the rats were randomly divided into control group, model group, western medicine group, and saikosaponin A group. The western medicine group was given 1.2 mg/kg/d of fluoxetine, and the saikosaponin A group was given 25 mg/kg/d of saikosaponin A, while the control group and model group were given the same volume of normal saline. The evaluation of depression in Rats was analyzed by Openfield-test and sugar water preference test. Flow cytometry was used to detect the expression of Th17 and Treg cells. And the expression of IL-17, IL-23, TNF-α, IL-10, TGF-βwere detected by enzyme-linked immunosorbent assay (ELISA). Results: Compared with the control group, the horizontal exercise score, vertical exercise score, and sugar preference of the model group decreased significantly (P <0.05). Compared with the model group, the above indicators were significantly increased in the western medicine group and saikosaponin A group (P <0.05). Flow cytometry showed that compared with the control group, the Th17 cells, Th17 / Treg cell ratio in model group increased significantly, whereas the Treg cells decreased significantly (P <0.05). Compared with the model group, The Th17 cells and Th17 / Treg ratio in western medicine group and saikosaponin A group decreased, while the Treg cells increased significantly (P <0.05). ELISA showed that compared with control group, the serum levels of IL-17, IL-23 and TNF-αin model group increased, while the levels of IL-10 and TGF-β decreased (P <0.05). Compared with model group, the levels of IL-17, IL-23 and TNF-αdecreased, while the levels of IL-10 and TGF-β increased in western medicine group and saikosaponin A group (P <0.05). Conclusion: Saikosaponin A can reduce the degree of depression by regulating the imbalance of Th17 / Treg cells and the secretion of inflammatory cytokines in depressed rats.