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

Nasr El-Din, Wael A; Abdel-Rahman, Gamal M; Abdel-Rahman, Alaa El-Din S; Kamel, Amr A

doi:10.21608/scumj.2013.45665

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

Document Type : Original Article

Authors

¹ Department of Anatomy, Faculty of Medicine, Suez Canal University, Egypt

² Department of Clinical Pathology, Faculty of Medicine, Suez Canal University, Egypt

³ Department of Pathology, Faculty of Medicine, Suez Canal University, Egypt

10.21608/scumj.2013.45665

Abstract

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 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 expressionwas 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.

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