牛膝多肽通过抑制氧化应激减轻大鼠心肌缺血/再灌注损伤

目的 探讨牛膝多肽（ABPP）预处理对心肌缺血/再灌注（MI/R）损伤的影响及其机制。方法 建立大鼠MI/R模型，将成年SD大鼠随机分为 Sham（假手术）组、MI/R组、药物预处理（ABPP＋MI/R）组。检测血流动力学、用氯化三苯基四氮唑和伊文思蓝双染法检测心肌梗死(MI)面积、以血浆肌酸激酶（CK）和乳酸脱氢酶（LDH）活性检测心肌损伤情况、以超氧化物、丙二醛（MAD）和超氧化物歧化酶（SOD）含量检测心肌氧化应激以及Western blot方法测定心肌组织中gp91phox的表达。用TUNEL法检测心肌细胞的凋亡指数(AI)，荧光分析法检测caspase 3活性。结果 与MI/R组比较，ABPP预处理使左心室上升、下降最大速率（±LVdP/dtmax）升高（P<0.05），MI面积显著减少〔MI/R组为（36.0±3.0）%，ABPP组为（26.5±3.5）%，P<0.05〕，血浆CK和LDH水平分别降低到（1251±72）U/L和（1961±122）U/L（P<0.05），TUNEL阳性染色显著降低（P<0.05），caspase-3的活性增加（P<0.05），超氧化物蓄积减少（P<0.05），显着降低了gp91phox的表达（P<0.05），MDA的含量显著减少（P<0.05），SOD活性增加（P<0.05）。结论 ABPP降低氧化应激和对MI/R损伤的心肌具有保护作用。

Achyranthes bidentata polypeptides reduce oxidative stress and exert protective effects against myocardial ischemic/reperfusion injury in rats

AIM To investigate the effects of achyranthes bidentata polypeptides (ABPP) preconditioning on myocardial ischemia/reperfusion (MI/R) injury and to explore the possible mechanism. METHODS Male Sprague Dawley (SD) rats were randomly divided into three groups: sham, myocardial ischemia reperfusion (MI/R) and ABPP+MI/R. The model of myocardial I/R injury in vivo was made by ligating the left anterior descending artery for 30 min followed by 4 h of reperfusion in SD rats. Hemodynamics were measured and myocardial infarct size was measured by Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. The level of hyperoxide superoxide, malondialdehyde (MDA) and plasma creatine kinase (CK) were measured and the activities of antioxidant enzyme superoxide dismutase (SOD) and lactate dehydrogenase (LDH) were detected. The gp91phox was determined by Western blot, cardiomyocyte apoptosis was detected using in situ TDT-mediated dUTP nick end labeling (TUNEL), activity of caspase-3 was determined by fluorescent assay and gp91phox was determined by Western blot. RESULTS Compared with those in the I/R group, left ventricular ±dp/dtmax in ABPP preconditioned rats increased significantly (P<0.05). The percentage of area of necrosis was reduced ［(36.0±3.0)% vs.(26.5±3.5)%, P<0.05］. Plasma CK and LDH levels decreased, respectively, to (1251±72) U/L and (1961±122) U/L (P<0.05 vs. MI/R). ABPP preconditioning decreased superoxide accumulation (P<0.05 vs. MI/R) and decreased gp91phox expression (P<0.05). Compared with those in the MI/R group, apoptosis index and expressions of caspase-3 were significantly attenuated in ABPP preconditioned animals (P<0.05). ABPP preconditioning markedly decreased gp91phox expression (P<0.05). CONCLUSION ABPP reduces oxidative stress and exerts cardioprotection against MI/R injury in rats.