摘要
目的探讨远隔缺血后处理(RIPC)对大鼠局灶性脑缺血再灌注损伤的保护作用,并观察RIPC对缺血再灌注损伤后内质网应激相关蛋白CRT、GRP78和caspase-12表达的影响。方法用线栓法制作大鼠大脑中动脉闭塞(MCAO)局灶性脑缺血再灌注模型,并进行远隔缺血后处理。再灌注6 h、12 h、24 h后分别采用Western blot检测CRT、GRP78和Bcl-2蛋白表达情况;RT-PCR检测caspase-12和caspase-3 mRNA表达情况。结果缺血再灌注组(6 h、12 h和24 h)与假手术组相比,CRT、GRP78、caspase-12、Bcl-2和caspase-3表达均升高,差异具有显著性(P<0.05)。远隔缺血后处理组与缺血再灌注组相比,CRT、GRP78和Bcl-2表达升高(12 h和24 h),差异具有显著性(P<0.05);caspase-12和caspase-3表达降低(6 h、12 h和24 h),差异具有显著性(P<0.05)。结论远隔缺血后处理可以减轻大鼠局灶性脑缺血再灌注产生的损伤,其保护作用机制可能与内质网应激反应有关。
Objective In the present study,we aimed to investigate effects of remote ischemic postconditioning on endoplasmic reticulum stress related factors of cerebral ischemia reperfusion injury. Methods A rat focal cerebral ischemia-reperfusion injury model was established using thread embolism method of middle cerebral artery occlusion（ MCAO）,and remote ischemic postconditioning intervention was conducted. The protein expression of CRT,GRP78 and Bcl-2 were assessed using Western blot and the mRNA expression of caspase-12 and caspase-3 were analyzed using RT-PCR after reperfusion 6 h,12 h,24 h respectively. Results Comparing with the sham operation group,the expression of CRT,GRP78,caspase-12,Bcl-2 and caspase-3 were significantly increased in the ischemia reperfusion group（ 6 h,12 h and 24 h）（ P〈0. 05）. Comparing with the Ischemia reperfusion group,the expression of CRT、GRP78 and Bcl-2 were significantly upregulated（ 12 h and 24 h） and the expression of caspase-12 and caspase-3 were significantly decreased（ 6 h,12 h and 24 h） in the remote ischemic postconditioning group（ P〈0. 05）. Conclusion Remote ischemic postconditioning can relieve ischemia-reperfusion brain injury in rats,and its possible mechanism of this protective effect may be associated with endoplasmic reticulum stress response.
出处
《中风与神经疾病杂志》
CAS
北大核心
2015年第4期336-339,共4页
Journal of Apoplexy and Nervous Diseases
基金
辽宁省科技厅基金(No.2014022006)
关键词
缺血再灌注
脑缺血
远隔缺血后处理
内质网应激
Isehemia-reperfusion
Cerebral ischemia
Remote ischemic posteonditioning
Endoplasmic reticulure stress
