Beneficial Effect of Stevenleaf on the Imbalance between Th17 and Treg in Nonalcoholic Fatty Liver Disease Model Rats

OBJECTIVE To study the effect of stevenleaf on improving non-alcoholic fatty liver disease in rat model and clarify mechanism from the point of immune-regulation. METHODS Forty-eight of rats were divided into six groups:normal group, model group, Essentiale (150 mg·kg^-1), high-dose (240 mg·kg^-1), moderate-dose (120 mg·kg^-1) and low-dose of stevenleaf (60 mg·kg^-1) groups. Rats were given high fat food for continuous 10 weeks, then given correspond drugs for 8 weeks. The levels of serum AST and ALT were measured at 0, 4 and 8 weeks experimental session. The rats were anesthetized after administration 8 weeks. The peripheral blood lymphocytes and serum were separated to measure the contents of Th17 and Treg cells in peripheral blood by flow cytometry and the levels of IL-17, IL-10 and TNF-α in serum by enzyme-linked immunosorbent assay (ELISA). HE staining was used to observe the pathological changes of liver tissue and immunohistochemistry to observe the positive expression of IL-17 and Foxp3 in liver tissue. RESULTS The 240 mg·kg^-1 of stevenleaf could reduce levels of serum ALT and AST after administration for 4 weeks (P<0.01). stevenleaf 240 mg·kg^-1, 120 mg·kg^-1 and 60 mg·kg^-1could reduce levels of serum ALT and AST after administration for 8 weeks (P<0.05, 0.01). Stevenleaf 240 mg·kg^-1 and 120 mg·kg^-1 could improve liver damage and reduce the level of TNF-α (P<0.05). Stevenleaf 240 mg·kg^-1 could reduce the content of IL-17 and increase IL-10 in serum (P<0.05, 0.01), reduce content of Th17 cell (CD4⁺IL-17⁺) and increase CD4⁺CD25⁺ Treg in peripheral blood lymphocytes (P<0.05), also significantly reduced the expression of inflammatory factor IL-17 and increased Foxp3 expression. CONCLUSION Stevenleaf could protect liver tissue damages, its mechanism may be related to regulating Treg/Th17 cell balance, reducing pro-inflammatory factors and increasing anti-inflammatory factors.