Interleukin-10 protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells Ac-tivation

Abstract EN

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 con-tractibility, 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 α-smooth 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.