基础医学与临床 ›› 2011, Vol. 31 ›› Issue (5): 503-508.

• 研究论文 • 上一篇    下一篇

缺血后适应调控树鼩脑缺血皮层TLR4表达

冯蕊1,李树清2   

  1. 1. 昆明医学院
    2. 昆明医学院病理生理教研室
  • 收稿日期:2010-11-22 修回日期:2011-03-03 出版日期:2011-05-05 发布日期:2011-05-06
  • 通讯作者: 李树清 E-mail:shuqing591@hotmail.com
  • 基金资助:
    缺血后适应机制研究;脑缺血机制研究;TLR4与脑缺血后适应脑内炎症反应

Ischemia postconditioning regulating TLR4 expression in Tree shrews’s cortex of thrombotic cerebral ischemia

Rui FENG,Shu-qing LI   

  1. Kunming Medical University
  • Received:2010-11-22 Revised:2011-03-03 Online:2011-05-05 Published:2011-05-06
  • Contact: Shu-qing LI E-mail:shuqing591@hotmail.com

摘要: 目的 探讨缺血后适应对皮层髓过氧化物酶(MPO)、TLR4表达及炎性反应的影响。方法 光化学法建立局灶性血栓性脑缺血模型;于脑缺血4h后夹闭右颈总动脉5min,再开夹5min,共3个循环建立缺血后适应模型。HE染色观察脑皮层组织学改变及炎性反应,MPO免疫组化染色、Westernblot法测定皮层TLR4蛋白表达,RT-PCR法测定皮层TLR4mRNA表达。结果 缺血4、24和72h后皮层神经元损伤及脑内炎性反应进行性加重,24h达高峰,后适应处理后损伤明显减轻,且炎性细胞浸润减少。脑缺血后MPO表达增强,后适应后24及72h表达减少(P<0.05)。脑缺血后TLR4蛋白表达升高(P <0.05),24h达高峰,后适应后4及24h表达减少(P<0.05),但后适应72h表达增加(P<0.05)。 TLR4mRNA的表达趋势与蛋白表达基本一致。结论 缺血后适应的脑保护机制可能与调控TLR4表达及抑制脑内炎性反应有关。

关键词: 光化学反应, 炎症, 脑缺血, Toll 样受体4, 缺血后适应

Abstract: Objective To investigate the effect of postconditioning after brain ischemia on the expresssion of MPO(myeloperoxidase)and TLR4(Toll-like receptor 4)and inflammation in cortex. Methods The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews, and ischemic postconditioning was established by 3 repeated cycles of 5 min of temporary right carotid artery clipped at 4h after the onset of photochemical reaction and 5 min reperfusion. The changes of histology of cortex (by Hematoxylin-and-eosin), MPO expression (by immunohistochemistry), TLR4 expression (by Western Blot Analysis) and TLR4 mRNA (by RT-PCR) were observed. Resulsts Our study found extensive neuronal injury and inflammation in cortex at 4, 24 and 72h, peak at 24h after the cerebral ischemia, while significantly attenuated after the postconditionng with less inflammation cells’ infiltration. Immunohistochemistry analysis showed that cerebral ischemia caused an increase in MPO expression in cortex, and ischemic postcondionting decreased the expression at 24h and 72h(P <0.05). Cerebral ischemia caused an increase of the TLR4 expression in cortex (P <0.05),peak at 24h. Postcondionting caused a decrease in the TLR4 expression in cortex at 4 hours and 24 hours(P <0.05), but an increase at 72 hours(P <0.05). The levels of TLR4 mRNA in cortex showed the similar variation trend in accordance with the protein expression. Conclusion The protection mechanisms of the prostconditioning may be associated with inhibitting inflammation and regulating TLR4 expression.

Key words: photochemistry, Inflammation, brain ischemia, toll-like receptor 4, postconditioning

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