Protective effect of polydatin against ischemia/reperfusion injury in rat heart.
Protective effect of polydatin against ischemia/reperfusion injury in rat heart.
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发表时间：
2008-04
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通讯作者：
Li-ping Zhang;Chang-ying Yang;Ying-Ping Wang;Fang Cui;Yi Zhang
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作者：
Li-ping Zhang;Chang-ying Yang;Ying-Ping Wang;Fang Cui;Yi Zhang
本研究旨在探讨虎杖苷对大鼠心肌缺血再灌注损伤的保护作用及其机制。在麻醉大鼠中，记录结扎和松开冠状动脉引起的缺血和再灌注心律失常，并测量心肌梗死面积。在Langendorff离体大鼠心脏中，记录全脑缺血30 min再灌注60 min前后的心功能。测定左室发展压（LVDP）、LVDP最大差值（±LVdp/dt（max））和冠脉流量（CF）。测定离体心脏超氧化物歧化酶（SOD）活性、丙二醛（MDA）、一氧化氮（NO）含量及一氧化氮合酶（NOS）活性。结果显示：（1）白藜芦醇苷组心律失常评分和心肌梗死面积明显低于对照组白藜芦醇苷组再灌注时LVDP、±LVdp/dt（max）和CF的恢复明显优于对照组虎杖苷组SOD活性显著高于对照组，MDA含量显著低于对照组虎杖苷组NO含量和NOS活性，尤其是组成型一氧化氮合酶（cNOS）活性均高于对照组（P<0. 05），NOS抑制剂L-NAME可逆转虎杖苷对缺血再灌注损伤的保护作用。提示虎杖苷对大鼠心脏缺血再灌注损伤具有保护作用。虎杖苷的心脏保护作用主要是通过cNOS介导的，其导致NO产生增加。
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 min 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/dt(max)) 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: (1) 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/dt(max) 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.