Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Background: Carbon tetrachloride (CCl4) is a critical hepatotoxicant causing liver injury and fibrosis via hepatic production of reactive oxygen species (ROS). Apigenin (APG) natural bioactive compound flavonoid antioxidant. We, therefore, evaluated whether APG could mitigate CCl4-mediated hepatotoxicity. Methods: Rats were randomly divided administered and/or CCl4 in Control group, + groups (APG: 10 20 mg/kg bw) 2 times per week for 7 consecutive weeks. Result: exposed to demonstrated marked increases serum alanine aminotransferase (ALT), aspartate (AST) monoamine oxidase (MAO) activities decreased malondialdehyde (MDA) level compared control. The superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) appreciably. intoxication caused significant inflammatory cytokines (IL-6 TNF-α) apoptosis markers, while the anti-inflammatory (IL-4 IL-10) with evident histopathological lesions APG-dose-dependently-prevented these alterations.