活性氧介导大剂量氯胺酮致原代培养皮层神经元凋亡

ROS mediates large dose of ketamine-induced apoptosis in cultured primary neuron

目的:观察活性氧(ROS)是否参与大剂量氯胺酮致原代培养皮层神经元凋亡。方法:单纯培养基(C组)、1mmol/L氯胺酮(K组)、1mmol/L氯胺酮复合2.5μmol/L超氧化物歧化酶类似物M40403(M组)分别作用于体外原代培养第6天的神经元24h,检测神经元ROS生成、凋亡细胞百分比及促凋亡蛋白Bax表达。结果:与C组相比,K组神经元ROS生成、凋亡细胞百分比、Bax表达分别是其1.7、4.2及2.0倍(P<0.05);与C组相比,M组神经元ROS生成、凋亡细胞百分比、Bax表达差异无统计学意义。结论:ROS介导大剂量氯胺酮致原代培养皮层神经元凋亡。

Objective：To observe whether reactive oxygen species（ROS） is involved in large dose ketamine-induced apoptosis on cultured primary neuron.Methods：Neuronal culture media （C group）,1 mmol /L ketamine （K group） or 1 mmol /L ketamine combined with 2.5 μmol /L superoxide dismutase mimetic M40403 （M group） was applied to primary neuron at day 6 for 24 h.Intraneuronal ROS production,the percentage of apoptotic cells and pro-apoptotic protein Bax expression were measured.Results：ROS production,the percentage of apoptotic cells and Bax expression in K group were 1.7,4.2,and 2.0-fold of those in C group,respectively （all P 0.05）.Compared with C group,M group had no statistically significant changes in ROS production,the percentage of apoptotic cells and Bax expression （all P 0.05）.Conclusion：ROS could mediate the apoptosis induced by large dose ketamine in cultured primary neuron.