动物造模,大鼠肾缺血再灌注 z-bio 2021-02-04 322

　　Objective: How to study the effect of vitamin E (vitamin E, VE) on myocardial injury after renal ischemia-reperfusion in rats?

　　Methods: Copy the rat RIR model, 4 weeks/kg/24h before reperfusion, give some animals VE500 mg, myocardial tissue malondialdehyde (MDA), myeloperoxidase (observe the change of MPO), yellow Purine oxidase (XO), superoxide dismutase (SOD), nitric oxide (NO) and plasma muscle. Acid kinase (CK) and creatine kinase isoenzyme (CK)-MB; mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricular systolic pressure (dp/dtmax) and dilatation are the largest Rate the left ventricular pressure drop (-dp/dtmax). Optical microscope? Immunohistochemical observation of myocardial morphology and endothelial nitric oxide synthase (eNOS) expression? Does Western blotting detect the expression of P47phox protein in cardiomyocytes?

　　Result: After the rat undergoes RIR, the MDA content, MPO and XO activity, SOD activity of myocardial tissue decrease, plasma CK? Under the microscope, does CK-MB increase, hemodynamic index decreases, myocardial cell edema, and NO concentration increases? The number of eNOS-positive cells increased, and the expression of p47phox protein increased. After VE administration, the myocardial tissue content, MPO and XO activity of MDA rats decreased, SOD activity increased, plasma CK-CK-MB decreased, hemodynamic index increased, and NO concentration increased. Myocardial damage under the microscope was reduced, and the number of eNOS-positive cells increased. , And the expression of p47phox protein decreased. Are the differences statistically significant?

　　Conclusion: VE may be anti-inflammatory, antioxidant, increased NO content, decreased P47phox expression, and other pathways after RIR.