动物造模,NADPH氧化酶 z-bo 2020-09-10 377

　　Objective: How to study the protective effect of Stephen Glycoside (TSG) that inhibits NADPH oxidase on cerebral ischemia-reperfusion (I/R) injury in mice?

　　Methods: 100 experimental mice were randomly divided into 5 groups: sham operation group model group, TSG low dose group (3 mg/kg), TSG medium dose group (6 mg/kg), TSG high dose group (12 mg) /kg), 20 animals per group. Two hours after cerebral ischemia, the mice were sacrificed by bilateral common carotid artery ligation, and the mice were sacrificed 24 hours after reperfusion. Mouse brain tissue was detected by HE staining for pathological examination, DHE staining and ESR spectrometer were used to detect the level of reactive oxygen species (ROS) in brain tissue, and the brain was detected by Western blotting. Has been completed. The expression of NOX4 and cleaved caspase-3/9 protein in the tissue?

　　Result: After cerebral ischemia and reperfusion in mice, severe pathological damage occurred in the cortical brain tissue of the ischemic area, and the level of ROS was significantly increased. Is the expression of NOX4 protein in brain tissue significantly up-regulated, and is the expression of apoptosis-related protein cleavedcaspase-3/9 protein significantly increased? TSG can significantly reduce the pathological damage of ischemia-reperfusion brain tissue in mice, inhibit the production of ROS, and significantly down-regulate the expression of oxidative stress protein NOX4, and the apoptosis-related protein cleavedcaspase-3 / it will significantly inhibit 9 Express?

　　Conclusion: TSG can reduce the production of reactive oxygen species by inhibiting the expression of oxidative stress protein NOX4 in brain tissues and inhibit the caspase- caspase- related to apoptosis. Can 3/9 overexpression prevent cerebral ischemia-reperfusion injury in mice?