〔Abstract〕 Objective To investigate the role and mechanism of PGC-1α-mediated mitochondrial biosynthesis in AMP-activated protein kinase(AMPK) agonist anti-hepatic ischemia-reperfusion injury(HIRI).Methods SD rats were randomly divided into Control group, HIRI group, HIRI+AICAR group, HIRI+SR-18292 group and HIRI+AICAR+SR-18292 group, with 8 rats in each group.The rats were intraperitoneally injected with AICAR(500 mg/kg) or SR-18292(32 mg/kg) before operation, and then the HIRI model was established by non-invasive vascular clamp clamping method.The samples were taken 24 hours after reperfusion.The contents of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in serum and the levels of malondialdehyde(MDA),superoxide dismutase(SOD) and adenosine triphosphate(ATP) in liver tissue were detected.HE staining was used to observe the pathological changes of liver tissue.The level of reactive oxygen species(ROS) and the changes of mitochondrial membrane potential in liver tissue were detected by fluorescence probe.The copy number of mitochondrial DNA(mtDNA) and the mitochondrial biosynthesis-related genes PGC-1α,NRF1,TFAM,UQCRC2 and other mRNA expression levels were detected by qRT-PCR.Western blot was used to detect the protein expression levels of AMPKα,p-AMPKα,mTOR,p-mTOR,PGC-1α and TFAM in liver tissue.Results Compared with the control group, the levels of ALT and AST in serum and MDA and ROS in liver tissue of rats in HIRI group increased, while the levels of SOD and ATP decreased(all P