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山东大学学报(医学版) ›› 2010, Vol. 48 ›› Issue (11): 46-49.

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步长脑心通对大鼠急性脑缺血再灌注小胶质细胞炎症反应和神经细胞凋亡的影响

赵清1,2,杨丽玲1, 杜怡峰1   

  1. 1.山东大学附属省立医院神经内科, 济南 250021; 2.淄博临淄齐都医院神经内科, 山东 淄博 255400
  • 收稿日期:2010-07-01 出版日期:2010-11-16 发布日期:2010-11-16
  • 通讯作者: 杜怡峰(1962- ),男,教授,博导,主要从事老年性痴呆、神经变性病以及脑血管病发病机制及防治研究。 E-mail:duyifengpmd2000@yahoo.com.cn
  • 作者简介:赵清(1975- ) ,女,硕士研究生,主治医师,主要从事脑血管病的研究。 E-mail:srhzqxd@126.com

Effect of the Buchang naoxintong capsule on apoptosis of neurons and inflammatory reaction of microglias after acute cerebral  ischemia-reperfusion injury in rats

ZHAO Qing1,2, YANG Li-ling1, DU Yi-feng1   

  1. 1. Department of Neurology, Affiliated Provincial Hospital of Shandong University, Jinan 250021, China;
    2. Department of Neurology, Qidu Hospital, Zibo 255400, Shandong, China
  • Received:2010-07-01 Online:2010-11-16 Published:2010-11-16

摘要:

目的    观察步长脑心通对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法    采用线栓法建立SD大鼠大脑中动脉阻塞(MCAO)再灌注模型,随机将30只大鼠分为假手术组、对照组、脑心通治疗组各10只,采用神经功能缺损评分对大鼠神经功能缺损程度进行评价,采用免疫组化和Western blot分别检测CD68、白细胞介素1β(IL-1β)的表达差异,并通过TUNEL、尼氏染色检测大鼠神经细胞的凋亡。结果    脑心通治疗组CD68、TUNEL、尼氏阳性细胞数及IL-1β的表达均较对照组明显减少(P<0.05),差异具有统计学意义。结论    脑心通能够明显减轻缺血再灌注损伤中脑组织的损伤程度,降低神经细胞的凋亡,其作用机制可能是通过抑制小胶质细胞激活导致的炎症介质释放,进而阻断缺血神经细胞的凋亡。

关键词: 缺氧缺血,脑;肿瘤坏死因子;白细胞介素1;炎症;大鼠,sprague-dawley

Abstract:

Objective    To study the effect of the Buchang naoxintong capsule on focal cerebral ischemia-reperfusion injury in rats and to investigate its corresponding mechanisms. Methods    A rat model of middle cerebral artery occlusion (MCAO) and reperfusion was established by I/R .Thirty rats were randomly divided into the sham operation group, the control group and the naoxintong-treated group, with 10 rats in each group. The neurological impairment score was used to evaluate the degree of neurological impairment of rats. Immunohistochemical stainning and Western blot were respectively used to detect expressions of CD68 and IL-1β. TUNEL and Nissl staining were used to detect neuron apoptosis in rats. Results    Activation of microglial cells, TUNEL- and nissl-positive cells, and expressions of CD68 and IL-1β in the naoxintong-treated group were obviously lower than those in the control group. The differences all had statistical significances(P<0.05). Conclusion     The Naoxintong capsule can significantly relieve the drgree of injury of brain tissues and depress apoptosis of neurocytes. The mechanisms could be that the Naoxintong capsule depresses activation of gitter cells which results in release of  inflammation mediators, and then prevents apoptosis of ischemic neurocytes.

Key words: Hypoxia-ischemia, brain; Tumor necrosis factor; Interleukin-1; Inflammation; Rats, sprague-dawley

中图分类号: 

  • R743.32
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