南方医科大学学报

南方医科大学学报 ›› 2006, Vol. 26 ›› Issue (06): 777-779.

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缺血再灌注损伤大鼠脑内神经巢蛋白的变化及通心络对它的影响

尹瑞雪； 陆兵勋； 王立新； 范建中； 卢昌均； 刘忆星；   

  1. 南方医科大学南方医院神经内科； 南方医科大学南方医院神经内科 广东广州510515； 广东广州510515；
  • 出版日期:2006-06-20 发布日期:2006-06-20
  • 基金资助:
    国家自然科学基金(30400612)~~

Nestin activation after rat cerebral ischemia-reperfusion injury and its changes in response to Tongxinluo treatment

YIN Rui-xue, LU Bing-xun, WANG Li-xin, FAN Jian-zhong, LU Chang-jun, LIU Yi-xing Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China   

  1. 南方医科大学南方医院神经内科； 南方医科大学南方医院神经内科 广东广州510515； 广东广州510515；
  • Online:2006-06-20 Published:2006-06-20

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摘要： 目的探讨神经巢蛋白(nestin)在脑缺血再灌注损伤后神经细胞的活化增殖情况及通心络对其影响。方法采用大鼠缺血再灌注损伤(MCAO)模型,应用免疫组织化学方法观察缺血后3、7、14以及21d缺血侧室管膜及室管膜下区(SVZ)、海马齿状回(HDG)神经巢蛋白的变化。给予模型大鼠通心络灌胃,观察神经干细胞增殖分化的变化。结果神经巢蛋白阳性细胞随缺血再灌注时间的延长,荧光强度值增加,第7、14、21天组与假手术组比较,差异具有显著性(P<0.05)。造模后通心络组BrdU阳性细胞荧光强度值和BrdU+nestin免疫双标荧光强度值均高于脑缺血再灌注模型组,差异显著(P<0.05)。结论大鼠缺血再灌注损伤后可引起其缺血侧SVZ、HDG区神经干细胞反应和增殖;而通心络可显著增加MCAO大鼠神经干细胞增殖分化能力。 

Abstract: Objective To investigate nestin activation in rat brain subjected to ischemia-reperfusion injury and its changes in response to Tongxinluo treatment. Methods Cerebral ischemia was induced by temporary middle cerebral artery occlusion (MCAO) in rats. At 3, 7, 14 and 21 days after MCAO, nestin expression in the ependyma, subventricular zone (SVZ), hippocampal subdentate gyrus zone (HDG) of the rats treated with Tongxinluo were guantified by immunohistochemistry. Results Compared with the sham operation group, nestin was significantly increased 7, 14 and 21 days after MCAO (P<0.05), and immunofluorescence of BrdU+nestin-positive neurons significantly increased in the SVZ. After treatment with Tongxinluo, the number of BrdU-positive neurons and BrdU+nestin-positive neurons significantly increased as compared with MCAO group (P<0.05). Conclusion Focal cerebral ischemia in the rat results in rapid response and proliferation of neural stem cells in the SVZ and HDG in the ischemic hemisphere, and Tongxinluo may enhance the differentiation and proliferation capacity of the neural stem cells after MCAO. 

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