The hepatoprotective effect of aspirin on carbon tetrachloride-induced hepatic fibrosis via inhibition of TGFβ-1 pathway and pro-inflammatory cytokines IL-1β and COX-2 in rats

Aspirin decreases liver fibrosis index and inflammation levels. However, the exact mechanism underlying the effects of aspirin are yet to be elucidated. The aim of the study was to investigate the potential protective effects of aspirin on carbon tetrachloride (CCl4)-induced hepatic fibrosis in Sprague-Dawley rats. Rats were divided into four groups, including healthy and CCl4 control and low-(aspirin 10 mg/kg + CCl4) and high-dose aspirin group (aspirin 300 mg/kg + CCl4). After 8 weeks treatment, the histopathological examinations of hepatocyte fibrosis in liver and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), IL-1 beta, transforming growth factor-beta 1 (TGF-beta 1), hyaluronic acid (HA), laminin (LN) and type IV collagen (IV.C) were determined. Histopathological examination suggested that aspirin decreased CCl4-induced hepatic fibrosis and liver inflammation. The high-dose aspirin group significantly decreased the serum levels of ALT, AST, HA and LN compared with the CCl4 control group. High-dose aspirin group significantly decreased the levels of pro-inflammatory cytokines IL-1 beta compared with CCl4 group. The high-dose aspirin group significantly inhibited the expression of TGF beta-1 protein compared with CCl4 group. Overall, the present study indicated that aspirin exhibited potent protective effects against CCl4-induced hepatic fibrosis via inhibition of the TGF beta-1 pathway and pro-inflammatory cytokine IL-1 beta.