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ERK1/2通路在缺血预处理大鼠大脑皮质的表达和作用
The expression and role of ERK1/2 in cerebral cortex of rats after brain ischemic preconditioning
【摘要】 目的探讨ERK1/2在大鼠脑缺血预处理中的表达及作用。方法采用大鼠大脑中动脉缺血再灌注损伤模型,随机分为假预处理组(Sham)和预处理组(BIP),各组又分4个亚组,每亚组6只动物。其中3个亚组分别于预处理或假预处理后15min、2h、24h用Western blot检测大脑皮质ERK1/2的表达。另外1个亚组在预处理或假预处理后24h栓塞左大脑中动脉2h,24h后行神经功能缺损评分,TTC染色法测脑梗死体积。结果预处理后15min、2h大脑皮质p-ERK1/2表达较强,与假预处理组相比有统计学意义(P<0.05),预处理后24h大脑皮质p-ERK1/2表达回落,与假预处理组相比无统计学差别(P>0.05)。两组预处理或假预处理后15min、2h、24h大脑皮质总ERK1/2表达无变化,组间相比无统计学差别(P>0.05);与假预处理组相比,预处理显著减少大脑中动脉栓塞导致的脑梗死体积(P<0.05)。预处理减少神经功能缺损。结论脑缺血预处理可能通过增强大脑皮质ERK1/2活性而保护皮质,减少脑梗死体积及神经功能缺损。
【Abstract】 Objective To explore the expression and role of ERK1/2 in cerebral cortex of rats after brain ischemic preconditioning(BIP).Methods All rats were divided into two groups randomly:sham group and BIP group.Each group was divided into four subgroups including 6 rats.Three subgroups’s ERK1/2 activation and expression in the cerebral cortex were examined by western blotting analysis at 15min,2h and 24h after BIP,the forth one was given a 2h left middle cerebral artery occlusion 24h after BIP or sham BIP.After 24h,the infarct volume was calculated by TTC staining and neurological function deficient was measured.Results Elevated p-ERK1/2 expression were observed 15min and 2h after preconditioning and had significant difference to sham group(P<0.05)and there were no different p-ERK1/2 expression in two groups 24h after BIP or sham(P>0.05).There were no different general ERK1/2 expression in two groups at 15min,2h and 24h after BIP or sham(P>0.05).BIP reduced infarct volume significantly than the sham BIP after MCAO(P<0.05).BIP reduced neurological function deficient.Conclusion BIP maybe protect cerebral cortex and reduce infarct volume as well as neurological function deficient through strengthening the activation of ERK1/2.
- 【文献出处】 中风与神经疾病杂志 ,Journal of Apoplexy and Nervous Diseases , 编辑部邮箱 ,2011年12期
- 【分类号】R743.3
- 【被引频次】2
- 【下载频次】148