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-1β, transforming growth factor-β1 (TGF-β1), 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-1β compared with CCl₄ group. The high-dose aspirin group significantly inhibited the expression of TGFβ-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 TGFβ-1 pathway and pro-inflammatory cytokine IL-1β.