Objective: To explore the effect of vitamin E (vitamin E, VE) on myocardial injury after renal ischemia reperfusion (RIR) in rats.
Methods: The rat RIR model was replicated, and some animals were given VE500mg/kg/24h by intragastric administration 4 weeks before reperfusion. The myocardial tissue was observed for malondialdehyde (MDA), myeloperoxidase (MPO), and xanthine oxidase (XO). 、Superoxide dismutase (SOD), nitric oxide (NO), plasma creatine kinase (CK) and creatine kinase isoenzyme (CK-MB) changes; measurement of mean arterial pressure (MAP), left ventricular contraction Pressure (LVSP), the maximum rate of increase in left ventricular pressure during systole (dp /dt max) and the maximum rate of decrease in left ventricular pressure during diastole (-dp /dt max); light microscope and immunohistochemical observation of myocardial morphology and endothelial monoxide Nitrogen synthase (eNOS) expression. Western blot method to detect the expression of P47phox protein in cardiomyocytes.
Results: After RIR in rats, the content of MDA, MPO and XO activity and NO concentration in myocardial tissue increased while SOD activity decreased, plasma CK and CK-MB increased, hemodynamic indicators decreased, myocardial cell edema, eNOS positive cells under microscope The expression of p47phox protein increased; after administration of VE, the MDA content, MPO and XO activity in rat myocardial tissue decreased, while SOD activity increased, plasma CK and CK-MB decreased, hemodynamic indicators increased, and NO concentration increased , Myocardial damage under the microscope was reduced, the number of eNOS positive cells increased, and the expression of p47phox protein decreased. The differences were statistically significant.
Conclusion: VE may exert a protective effect on myocardium after RIR through anti-inflammatory, anti-oxidant, increasing NO content, and reducing P47phox expression.