| 彭文娟,杨剑文,刘湘玉,杨期明.阿托伐他汀对大鼠脑缺血再灌注PERK/elfR2a通路及Caspase-3表达的影响.[J].中南医学科学杂志.,2016,(1):20-24. |
| 阿托伐他汀对大鼠脑缺血再灌注PERK/elfR2a通路及Caspase-3表达的影响 |
| The Study of PERK/eIF2a Pathway and the Expression of Caspase-3 in Ischemia-reperfusion Rats and Atorvastatin Intervention |
| 投稿时间：2015-10-08 修订日期：2015-11-26 |
| DOI： |
| 中文关键词: 蛋白激酶R样内质网激酶 eIF2a 内质网应激 Caspase-3 局灶性脑缺血再灌注 阿托伐他汀 |
| 英文关键词:protein kinase-like ER kinase EIF2a endoplasmic reticulum stress Caspase-3 ischemia reperfusion atorvastatin |
| 基金项目:湖南省卫生计生委资助项目(B2015-73). |
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| 中文摘要: |
| 目的 研究蛋白激酶R样内质网激酶(PERK)/eIFR2a通路及Caspase-3在大鼠脑缺血再灌注损伤中的作用机制及阿托伐他汀对其的影响。方法采用大脑中动脉线栓塞法制作大鼠脑缺血再灌注模型；随机分为缺血再灌注组、假手术组、阿托伐他汀组、阿托伐他汀+Salubrinal抑制剂组,大体标本采用TTC染色,釆用Western-blot法检测PERK、Caspase-3蛋白表达及eIF2a蛋白磷酸化。结果与假手术组相比,大鼠缺血再灌注后PERK蛋白表达及eIF2a 的磷酸化增加, Caspase-3表达的活性增强(P<0.01)；阿托伐他汀干预可以减轻PERK蛋白表达及eIF2a蛋白磷酸化(P<0.05)。给予特异性eIF2a磷酸化抑制剂Salubrinal后可抑制eIF2a的磷酸化及Caspase-3表达的活性(P<0.05),对PERK蛋白表达无影响。形态学上从TTC染色提示:在缺血再灌注组TTC染色可见大片脑梗死组织。Salubrinal抑制剂及阿托伐他汀干预后脑梗死体积明显缩小(P<0.05)。结论内质网应激通过PERK/eIF2a/Caspase-3途径促进细胞凋亡,阿托伐他汀干预可以减轻脑缺血再灌注损伤。 |
| 英文摘要: |
| Objective To study the PERK/eIF2a pathways and Caspase 3 in the mechanism of action of ischemia reperfusion injury in rats and the effect of atorvastatin.MethodsProduce the ischemia reperfusion model rats by Middle cerebral artery embolism method which were divided into the ischemia reperfusion group,control group,atorvastatin intervention group and eIF2a suppression group.To observe the changes of ischemic brain,specimens were treated with TTC staining,the PERK,Caspase-3 protein expression and protein phosphorylation eIF2a were detected by western-blot.ResultsCompared with the control group,after ischemia reperfusion,PERK protein expression and protein phosphorylation eIF2a increased,the expression of Caspase 3 was enhanced,and the expression of PERK protein and phosphorylation eIF2a was relieved after atorvastatin intervention.The expression of Caspase-3 and phosphorylation eIF2a was inhibited by inhibitor Salubrinal,which had no effect no PERK.Large cerebral infarction in ischemia reperfusion group was visible by TTC staining after ischemia reperfusion.Cerebral infarction volume was significantly narrowed by atorvastatin intervention or inhibitor Salubrinal.ConclusionCell apoptosis was related to the PERK/ eIF2a /Caspase 3 pathways after endoplasmic reticulum stress,atorvastatin can reduce the damage of cerebral ischemia reperfusion. |
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