ABSTRACT
OBJECTIVE To investigate the effects of astilbin （AST） on myocardial ischemia-reperfusion injury （MIRI） in rats and its potential mechanism. METHODS SD male rats were randomly divided into sham operation group， model group， positive control group （Compound Salvia miltiorrhiza tablets， 240 mg/kg）， AST low-dose and high-dose groups （30， 90 mg/kg）， and high- dose of AST+hypoxia-inducible factor-1α（HIF-1α） inhibitor group （AST 90 mg/kg+2ME2 15 mg/kg）， with 25 rats in each group. Except for sham operation group， MIRI model was induced in other groups， and then given relevant drug or normal saline intragastrically or intraperitoneally， for consecutive 28 d. Serum contents of cardiac troponin I （cTnI） and creatine kinase isoenzyme （CK-MB） were detected； volume ratio of myocardial infarction was measured； the pathological changes of myocardium， the apoptotic rate of myocardial cells and ultrastructure of mitochondria in myocardial tissue were all observed. The contents of tumor necrosis factor α （TNF-α）， interleukin 6 （IL-6） and malondialdehyde （MDA）， the activity of superoxide dismutase （SOD）， the expressions of HIF-1α， adenovirus E1B interacting protein 3 （BNIP3） and myosin-like Bcl-2 interacting protein （Beclin1） were determined in myocardium. The ratio of microtubule-associated protein light chain 3 （LC3） Ⅱ to Ⅰ （LC3 Ⅱ/Ⅰ） in rat myocardium was calculated. RESULTS Compared with model group， no obvious swelling was found in the myocardial tissue of rats in positive control group， AST low-dose and high-dose groups， and the myocardial fibers were arranged regularly； the volume ratio of myocardial infarction， the contents of cTnI， CK-MB， TNF-α， IL-6 and MDA， the apoptotic rate were decreased significantly （P＜0.05）， while SOD activity， protein expressions of HIF-1α， BNIP3 and Beclin1， LC3Ⅱ/Ⅰ were increased significantly （P＜0.05）. HIF-1α inhibitor could significantly weaken the improvement effect of AST on the above indicators in MIRI model rats （P＜0.05）. CONCLUSIONS AST enhances mitochondrial autophagy by activating HIF-1α/BNIP3 signaling pathway， thereby reducing MIRI in rats.
ABSTRACT
Objective To investigate the effects of nicardipine on apoptosis in ischemia?reperfusion myocardium of rabbits. Methods Forty New Zealand rabbit were randomly divided into 4 groups:control group(group A),ischemia group(group B),ischemia?reperfusion group(group C),ni?cardipine treatment group(group D). Ischemia?reperfusion model was established by left circumflex branch coronary artery ligation for 40 min,fol?lowed by 120 min reperfusion. Apoptotic cardiomyocyte was detected using the analysis for the exposure of phosphatidyl?serine ( Annexin V)meth?od. Results Myocardial cell damage was lower in D group than that in group B and group C from pathology(P0.05). Conclusion Nicardipine horizon can reduce the myocardial cell apoptosis in rabbits with myocardial ischemic reperfusion injury.