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目的 研究脑缺血再灌注期间海马CA1区锥体细胞微管运动蛋白活性的变化。方法 沙土鼠前脑缺血再灌注模型 ,脑缺血 10min。将 2 0只沙土鼠随机分为 4组 (n =5 ) :假手术组、再灌注Ⅰ组 (再灌注 6h)、再灌注Ⅱ组 (再灌注 48h)、再灌注Ⅲ组 (再灌注 96h)。采用免疫组织化学方法结合计算机图像分析测定脑缺血再灌注期间海马神经元微管运动蛋白活性。结果 脑缺血再灌注期间海马CA1区微管运动蛋白活性明显下降 ,在再灌注 6h、48h、96h时其活性分别仅为假手术组的 49%、32 %和 12 % (P <0 .0 1)。而CA2、CA3、CA4区微管运动蛋白活性无明显变化。在再灌注 48～ 96h ,CA1区大多数神经元出现变性坏死。结论 脑缺血再灌注可导致海马CA1区微管运动蛋白活性进行性下降 ,其可能是发生延迟性神经元死亡的主要原因。
Objective To study the changes of the microtubule motor protein in hippocampal CA1 pyramidal cells during cerebral ischemia-reperfusion in rats. Methods The gerbil model of forebrain ischemia-reperfusion, cerebral ischemia 10 min. 20 gerbils were randomly divided into 4 groups (n = 5): sham operation group, reperfusion group Ⅰ (reperfusion 6h), reperfusion group Ⅱ (reperfusion 48h), reperfusion group Ⅲ (reperfusion 96h) . Immunohistochemistry and computer image analysis were used to determine the microtubule motor protein activity of hippocampal neurons during cerebral ischemia-reperfusion. Results The activity of microtubule motor protein in hippocampal CA1 area was significantly decreased during cerebral ischemia / reperfusion, and the activity of microtubule was only 49%, 32% and 12% of the sham operation group at 6h, 48h and 96h after reperfusion (P <0. 1). The activity of microtubules in CA2, CA3 and CA4 showed no significant change. At 48-96h after reperfusion, most neurons in CA1 area degenerated and necrotic. Conclusions Cerebral ischemia-reperfusion can lead to the progressive decline of microtubule motor protein in hippocampal CA1 region, which may be the main reason of delayed neuronal death.