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作 者:张利萍[1] 杨长瑛[1] 王莹萍[1] 崔芳[1] 张翼[1]
机构地区:[1]河北医科大学基础医学院生理学教研室,石家庄050017
出 处:《生理学报》2008年第2期161-168,共8页Acta Physiologica Sinica
摘 要:本文利用冠脉结扎/放松方法和Langendorff灌注技术,建立在体和离体大鼠心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤模型,探讨白藜芦醇甙(polydatin)对大鼠I/R心肌损伤的保护作用及其机制。观察白藜芦醇甙对缺血和再灌注心律失常、心肌梗死面积、心脏收缩功能、心肌超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量、NO含量以及一氧化氮合酶(nitric oxide synthase,NOS)活性的影响。结果显示:与对照组相比,白藜芦醇甙组大鼠缺血和再灌注心律失常明显降低(P<0.05,P<0.01);心肌梗死面积显著减少(P<0.01);I/R心脏左心室发展压(left ventricular developedpressure,LVDP)、左心室压力上升和下降最大变化速率(±LVdp/dtmax)、冠脉流量(coronary flow,CF)明显改善(P<0.05,P<0.01);心肌SOD活性升高,MDA含量降低(P<0.05);NO含量和NOS及cNOS活性也明显升高(P<0.05);此外,NOS抑制剂L-NAME拮抗白藜芦醇甙对I/R心肌的保护作用。结果提示:白藜芦醇甙具有明显的抗心肌I/R损伤作用,此作用主要由cNOS产生的NO增加所介导。The aim of the present study was to investigate the protective effect of polydatin against myocardial ischemia/reperfusion injury in rats and the underlying mechanism. In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosing the coronary artery was recorded and myocardial infarct size was measured. In Langendorff isolated rat heart, cardiac function was recorded before and after 30 rain of global ischemia followed by 60 min of reperfusion. The parameters of cardiac function include left ventricular developed pressure (LVDP), maximal differentials of LVDP (±LVdp/dtmax) and coronary flow (CF) were measured. Myocardial superoxide dismutase (SOD) activity, the contents of myocardial malondialdehyde (MDA) and nitric oxide (NO) as well as the activity of nitric oxide synthase (NOS) were measured in isolated heart. The results showed: (l) Arrhythmia score and myocardial infarct size were significantly lower in polydatin group than that in the control group (P〈0.05, P〈0.01); (2) The recovery of LVDP, ±LVdp/dtmax and CF during reperfusion in polydatin group were significantly better than that in the control rats (P〈0.05, P〈0.01); (3) SOD activity in polydatin group was significantly higher than that in the control group, but MDA content was lower in polydatin group than that in the control group (P〈0.05); (4) NO content and NOS activity, especially constitutive nitric oxide synthase (cNOS) activity in polydatin group were higher than that in the control group (P〈0.05); (5) L-NAME, the NOS inhibitor, reversed the protective effect of polydatin against ischemia/reperfusion injury. The results suggest that polydatin has a protective effect against ischemia/reperfusion injury in rat heart. The cardioprotection of polydatin is mainly mediated by cNOS which leading to an increase in NO production.
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