The liver carries out many essential tasks, such as synthesising cholesterol, controlling the body’s
storage of glycogen, and detoxifying metabolites, in addition to performing, and regulating
homeostasis. Hepatic fbrosis is a pathological state characterized by over accumulation of
extracellular matrix (ECM) including collagen fbers. Sildenafl (a selective inhibitor of type 5
phosphodiesterase) has antiinfammatory, antioxidant and antiapoptotic properties. It is
commonly used to treat erectile dysfunction in male. The purpose of the current investigation was
to evaluate sildenafl’s hepatoprotective potential against liver fbrosis in rats that was caused by
carbon tetrachloride (CCl4). Liver enzymes and oxidative markers as well as profbrotic genes were
determined. The fndings showed that sildenafl alleviates the hepatic dysfunctions caused by
CCl4 by restoring normal levels of ALT, AST, and GGT as well as by restoring the antioxidant status
demonstrated by increased glutathione (GSH), and catalase. In addition, a signifcantly down
regulated the mRNA expressions of profbrotic genes [collagen1α, IL1β, osteopontin (OPN), and
transforming growth factorβ (TGFβ)]. Additionally, sildenafl lessens the periportal fbrosis between
hepatic lobules, congestion and dilatation in the central vein, and the infammatory cell infltrations.
As a result, it is hypothesized that sildenafl may be helpful in the management of hepatotoxicity
brought on by CCl4 through suppressing OPN.