2-4脱氧葡萄糖在内质网应激预处理诱导脑缺血耐受中的作用

Effect of 2-deoxyglucose on cerebral ischemia tolerance after endoplasmic reticulum stress preconditioning

目的观察2-脱氧葡萄糖(2-DG)诱导内质网应激(ERS)预处理时GRP78、Bcl-2、Bax的变化,探讨2-DG在脑缺血耐受中的作用。方法将64只SD大鼠随机均分为假手术组(SH组)、缺血/再灌注组(I/R组)、ERS预处理组(IP组)、IP+I/R组。采用原位末端标记法检测海马CA1区凋亡细胞,免疫组化法、Western-Blot法检测GRP78、Bcl-2及Bax蛋白在海马CA1区的表达。结果与I/R组比较,IP+I/R组GRP78、Bcl-2蛋白表达升高,Bax蛋白表达及细胞凋亡明显减少(P<0.05或<0.01)。结论 2-DG上调GRP78时也上调Bcl-2表达,减轻神经细胞凋亡,起到脑保护作用;2-DG可抑制Bax表达,减弱其对神经细胞的损害,使细胞存活。

Objective To observe the changes of GRP78,Bcl-2 and Bax when pretreating by endolasmic reticulum stress（ERS） induced by 2-deaeration glucose（2-DG）,and investigate the function of 2-DG in the cerebral ischemic tolerance.Methods A total of 64 SD rats was randomly divided into sham group（SH）,ischemia/reperfusion group（I/R）,endoplasmic reticulum stress preconditioning group（IP）,IP＋I/R group（IP＋I/R）.In hippocampal CA1 area,using TUNEL to test cell apoptosis,using immunohistochemistry and Western-Blot to detect the levels of GRP78,Bcl-2 and Bax.Results Compares with the I/R group,GRP78 and the Bcl-2 levels in IP＋I/R group increased,Bax levels and the pyramidal cells of apoptosis reduced（P0.05 or0.01）.Conclusions 2-DG can elevate the levels of GRP78,Bcl-2,reduce neuronal cell apoptosis,and it plays the brain protective function;2-DG may suppress the Bax express,weaken the harm to nerve cells,and make the cell survive.