动物造模 Z-bio 2022-12-27 285

　　Objective Microcystin pollution caused by cyanobacteria blooms is one of the topics of worldwide concern. Microcystin LR (MC-LR) has strong specific hepatotoxicity, but the exact mechanism of causing liver damage has not been fully clarified. To solve this problem, this study explored the molecular mechanism of MC-LR induced mitochondrial function changes in hepatocytes from the cellular and molecular level.

　　Methods Primary mouse hepatocytes were extracted and gradient dose of MC-LR (2 5~10 nmol/L) for 48 h, and the control group without toxin was used to detect the effect of MC-LR on mitochondrial function (including ATP level and mitochondrial membrane potential), DNA damage (including comet assay and 8-OHdG level), and analyze the p53 inhibitor pft- α Mitochondrial function damage.

　　Results MC LR caused mitochondrial dysfunction, DNA damage and up regulation of p53 protein expression in hepatocytes; P53 specific inhibitor pft- α Reduce mitochondrial damage caused by MC-LR.

　　Conclusion Under the experimental conditions, the mechanism of MC-LR induced mitochondrial dysfunction in mouse liver cells is related to its DNA damage and p53 up regulation.