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Background: After liver injury, hepatic stellate cells (HSCs) lose vitamin A and transform into myofibroblasts (MFB), called activated HSCs, which express α-SMA and have the function of contractibility, proliferation, and fibrogenesis. IL-10 is active as an antifibrogenic drug able to reduce the α-SMA expression in ongoing fibrogenesis. Aim: To study the effect of interleukin-10 on the expression of α-smooth muscle actin (α-SMA), in hepatic stellate cells of experimental rats with hepatic fibrosis. Materials and Methods: one hundred and eight rats were divided equally into two groups: control and CCl4-treated group, which subdivided into 3 subgroups, a group immediately puts into death after treatment, spontaneous recovery (SR) group, and IL-10-treated group. Each group included 27 rats. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin were assessed. Livers were taken out and processed for the expression of tissue αsmooth muscle actin (α-SMA) by immunohistochemical assay. Results: serum ALT and AST were significantly higher in rats injected with CCl4 (90.01±2.77 IU/L and 56.42±3.27 IU/L, P < 0.05 each), moderately reduced in the SR group (58.26±1.94 IU/L and 37.18±2.31IU/L, P < 0.05 each), and significantly reduced by administration of IL-10 (28.77±2.03IU/L and 37.18±2.31 IU/L, p< 0.05 each). The expression of α-SMA in the hepatic cells was strong in CCl4-induced fibrosis group compared to the control group (p< 0.05). The expression was moderate in the spontaneous recovery group, but less than CCl4-treated group and was significantly reduced in IL-10-treated group. Conclusions: IL-10 is an active antifibrogenic drug that reduces α-SMA expression in ongoing fibrogenesis.

Interleukin-10 Protects Rat Liver from CCl4-induced Fi-brogenesis via Inhibition of Hepatic Stellate Cells Activation