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目的观察ATP敏感性钾通道(KATP)开放剂尼可地尔(nicorandil)对大鼠脑缺血/再灌注(I/R)损伤的保护作用及其机制。方法将60只雄性Wistar大鼠随机分为4组:A组(假手术组)、B组(脑缺血再灌注组)、C组(脑缺血再灌注+尼可地尔组)及D组(脑缺血再灌注+尼可地尔+5-HD组),采用线栓法建立大鼠大脑中动脉闭塞(MCAO)模型,各组于脑缺血2h后进行再灌注,再灌注22h后观察各组大鼠神经功能评分、脑梗死体积、线粒体标志酶活性和脂质过氧化降解产物丙二醛(malondialdehyde,MDA)的含量。结果(1)B、C、D组再灌注22h后神经功能评分显著低于A组,脑梗死体积、脂质过氧化物MDA含量均显著高于A组,线粒体标志酶活性SDH、CO表达显著低于A组(P<0.01);(2)与B、D组比较,C组神经功能评分明显升高,脑梗死体积、MDA含量明显减少,SDH、CO活性明显增高(P<0.01);(3)B组和D组各指标之间比较差异均无显著性(P>0.05)。结论尼可地尔对大鼠脑缺血再灌注损伤具有保护作用,其机制可能与开放mitoKATP通道、维护线粒体功能、减少氧自由基产生有关。
Objective To observe the protective effect of nicorandil, an ATP sensitive potassium channel (KATP) opener, on cerebral ischemia / reperfusion (I / R) injury in rats and its mechanism. Methods Sixty male Wistar rats were randomly divided into 4 groups: group A (sham operation group), group B (cerebral ischemia reperfusion group), group C (cerebral ischemia reperfusion + nicorandil group) and D (MCAO) model was established by thread occlusion. The rats in each group were reperfused 2 hours after cerebral ischemia and reperfused for 22 hours Neurological function score, infarct volume, mitochondrial enzyme activity and malondialdehyde (MDA) content in rats were observed. Results (1) The scores of neurological function in group B, C and D after reperfusion for 22h were significantly lower than those in group A, and the volume of cerebral infarction and the content of MDA in lipid peroxidation were significantly higher than those in group A (P <0.01); (2) Compared with B and D groups, the scores of neurological function in group C were significantly increased; the volume of cerebral infarction and the content of MDA were significantly decreased; the activities of SDH and CO were significantly increased (P <0.01); (3) There was no significant difference between each index of group B and group D (P> 0.05). Conclusions Nicorandil may have a protective effect on cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the opening of mitoKATP channels, the maintenance of mitochondrial function and the reduction of oxygen free radicals production.