| 引用本文:张晓燕，杨金升，谷有全，石向群.脑心通对脑缺血再灌注损伤细胞外信号调节激酶活化的影响[J].世界中医药,2007,2(3):. |
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| 脑心通对脑缺血再灌注损伤细胞外信号调节激酶活化的影响 |
| Effect of Naoxintong on Activation of Extracelluar Signal Regulated Kinases after Cerebral Ischemia/Reperfusion Injury in Rats |
| 投稿时间：2007-02-08 |
| DOI： |
| 中文关键词: 脑缺血 细胞外信号调节激酶 @ 脑心通 |
| English Keywords:Cerebral ischemia Extracellular signal regulated kinase @ Naoxintong |
| 基金项目: |
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| 中文摘要: |
| 目的：观察大鼠局灶性脑缺血/再灌注(ischemia/reperfusion，I/R)后信号转导介质细胞外信号调节激酶(extracellular signal-regulated kinase，ERK)的活化情况以及脑心通对其的影响。方法：雄性成年Wistar大鼠90只，随机分成3组：假手术组、对照组和脑心通组(每组30只)，分别于缺血前6日每日用生理盐水4ml、和脑心通0.48g/kg(4ml生理盐水溶解)灌胃。采用线栓法致大脑中动脉栓塞(middle cerebral artery occlusion，MCAO)模型，在脑缺血再灌注后的3h、6h、24h、48h和72h分别处死大鼠(各组每个时间点6只)，将脑组织进行免疫组织化学、TTC染色，TUNEL法观察细胞凋亡。结果：脑缺血诱导ERK活化，第6h达高峰，并持续到72h。脑心通组ERKｓ活化明显较对照组增强，而且各时间点ERK免疫反应阳性细胞数脑心通组较对照组显著增多(P<0.01)。脑心通组TTC染色梗死体积及凋亡细胞数较对照组明显较少(P<0.01)。结论：局灶性脑缺血再灌注可诱导缺血脑细胞部分ERK活化，脑心通干预可使缺血大脑海马ERK活化增强,减轻细胞的缺血性损伤。 |
| English Summary: |
| To study the activation of extra-cellular signal regulated kinase (ERK) after focal cerebral ischemia/reperfusion in rats and effect of Naoxintong on it.Methods：Ninety male adult wistar rats were randomly divided into 3 groups，the sham-operated group、the control group and the Naoxintong group．The model of middle cerebral artery occlusion (MCAO) was established by introducing a nylon suture to the right internal carotid artery. Before the ischemic phase, to rats in the sham-operated group and the control group, 4ml of normal saline was intragastric administrated, and to rats in the Naoxintong group, Naoxintong dissolved in 4ml of normal saline(0.48g/kg) was intragastric administrated for 6 days. The rats were decapitated at 3hrs, 6hrs, 24hrs, 48hrs, 72hrs after reperfusion.6 rats of every group at each time point. The volume of infarction were observed by the TTC staining method;The apoptosis neurons were detected in CA1area by TUNEL method ;ERK phosphorylation was detected by immunohistochemistry.Results：The cerebral ischemia induced ERK activation reached the peak at 6hrs and maintained to 72hrs after reperfusion.As compared with the control group,the ERK activation in the Naoxintong group was significantly enhanced with increased positive immune reacted cells(P<0.01). As compared with the control group,the volume of infarction and the apoptosis neurons in the Naoxintong group was significantly decreased(P<0.01). Conclusion：Cerebral ischemia/reperfusion could induce the activation of ERK in the ischemic brain cells,untervention of Naoxintong could enhance the activation and decrease the volume of infarction and the apoptosis neurons ,alleviate the ischemic injury. |
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