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目的研究2-脱氧葡萄糖(2-DG)诱导内质网应激(ERS)预处理对大鼠脑缺血再灌注的保护作用。方法 64只雄性SD大鼠随机均分为假手术组(SH组)、缺血/再灌注组(I/R组)、2-DG诱导的ERS预处理组(IP组)、IP+I/R组。采用TUNEL法检测CA1区凋亡细胞,免疫组化法、Western-Blot法检测p-JNK蛋白在海马CA1区的表达变化。结果与对照组比较,I/R组海马CA1区锥体神经元排列紊乱及变性坏死,形态正常椎体细胞百分数减少,凋亡细胞数目明显增加,脑组织p-JNK表达水平增加;与I/R组相比,IP+I/R组形态正常锥体细胞明显增加,凋亡细胞数目明显减少,脑组织表达较I/R组明显减少。结论 2-DG诱导的ERS对脑缺血再灌注损伤有保护作用,可能与其抑制细胞凋亡和p-JNK表达相关。
Objective To investigate the protective effect of 2-deoxyglucose (2-DG) -induced endoplasmic reticulum stress (ERS) preconditioning on cerebral ischemia-reperfusion in rats. Methods Sixty-four male Sprague-Dawley rats were randomly divided into sham operation group (SH), ischemia / reperfusion (I / R) group, 2-DG induced ERS preconditioning group R group. The apoptotic cells in CA1 area were detected by TUNEL method. The expression of p-JNK protein in hippocampal CA1 area was detected by immunohistochemistry and Western-Blot. Results Compared with the control group, pyramidal neurons in the hippocampal CA1 region of I / R group were disordered and degenerated and necrotic. The percentage of normal vertebral cells decreased, the number of apoptotic cells increased and the expression of p-JNK in brain increased. Compared with the I / R group, the number of apoptotic cells and the number of apoptotic cells in the IP + I / R group were significantly increased compared with the I / R group. Conclusions 2-DG-induced ERS may have a protective effect on cerebral ischemia-reperfusion injury, which may be related to the inhibition of apoptosis and the expression of p-JNK.