动物造模 z-bio 2022-04-22 611

　　Objective Microcystin contamination caused by cyanobacterial blooms is one of the worldwide concerns. Microcystin LR (MC-LR) has strong specific hepatotoxicity, but its exact mechanism of liver injury has not been fully elucidated. To solve this problem, this study explored the molecular mechanism of MC-LR-induced changes in mitochondrial function of hepatocytes from the cellular and molecular level.

　　Methods The mouse primary hepatocytes were extracted and treated with gradient doses of MC-LR (2. 5 ~ 10 nmol/L) for 48 h. The control group without toxin was used as a control to detect the effect of MC-LR on mitochondrial function (including MC-LR). ATP level and mitochondrial membrane potential detection), DNA damage (including comet test and 8-OHdG level detection), and analysis of mitochondrial function damage under the action of p53 inhibitor pft-α.

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

　　Conclusions Under the experimental conditions, the mechanism of MC-LR causing abnormal mitochondrial function in mouse hepatocytes is related to the up-regulation of p53 induced by DNA damage.