2-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

摘要

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-IDG in the cerebral ischemic tolerance. Methods A total of 64 SD rats was randomly divided into sham group (SH), ischemia/reperfusion group (l/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 ( P ＜ 0.05 or ＜ 0.01 ). 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.%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.