依达拉奉通过抑制内质网应激途径对谷氨酸刺激神经元损伤的保护作用

摘要

目的 研究依达拉奉通过抑制内质网应激(ERS)途径对氧化应激损伤神经元的保护作用.方法 神经元原代培养鉴定后分为谷氨酸刺激组(A组)、依达拉奉预处理组(B组)和空白对照组(C组).流式细胞术检测细胞凋亡率,免疫荧光观察半胱天冬氨酸蛋白酶12 (Caspase-12)表达的变化,Western blot检测蛋白激酶R样内质网激酶(PERK)和Caspase-12的蛋白表达.结果 与C组相比,A组细胞凋亡率、PERK及Caspase-12的表达均明显增加(P＜0.05)；而B组能显著抑制A组各观察指标的增加过程(P＜0.05).结论 依达拉奉可能通过抑制ERS途径降低神经元的凋亡,从而对神经元起保护作用.%Objective To investigate the protective effect of edaravone on glutamate-induced neuron damage by inhibiting endoplasmic reticulum stress (ERS).Methods Primary neurons were identified and divided into three groups of A(stimulated with glutamate 100 μmol/L),B(pretreated with edaravone 500 μmol/L before stimulation of glutamate 100 μmol/L) and C(blank controls).The rate of cell apoptosis was determined by flow cytometry,and the change of Caspase-12 expression was detected by immunofluorescence.The protein expressions of PERK and Caspase-12 were detected by Western blot.Results Compared with group C,the rate of cell apoptosis and expressions of PERK and Caspase-12 were significantly increased in group A(P＜0.05),which were all obviously inhibited in group B(P＜0.05).Conclusion Edaravone decreases neuron apoptosis probably via inhibiting ERS and protects the damaged neuron.