Hepatoprotective effect of galangin on carbon tetrachloride-induced hepatotoxicity via the LKB1/AMPK pathway

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl 4 ) in mice. Mouse hepatotoxicity model was established intraperitoneal injection (i.p.) 10 ml/kg body weight CCl that diluted with corn oil to a proportion 1:500 Kunming The mice were randomly divided into five groups named control group, and 1, 5, mg/kg group. levels alanine aminotransferase (ALT) aspartate (AST) analyzed ELISA. Liver histopathological examination observed via optical microscopy. superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathion (GSSG) assess oxidative stress. Finally, western blot assay carried out analyse expression total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), B1 (LKB1), phospho-LKB1 (p-LKB1). Compared AST, ALT, MDA, GSSG increased significantly ( p < 0.01); activity SOD GSH decreased revealed necrosis. However, treatment (5 mg/kg) reversed these -induced damage indicators. Furthermore, (10 p-AMPK p-LKB1 0.01). This study supports hepatoprotective effect against hepatotoxicity, perhaps occurring mainly through LKB1/AMPK-mediated pathway.