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目的研究线粒体内膜ATP敏感性钾通道(Mito-KATP)特异性开放剂二氮嗪预处理对缺氧复氧后大鼠海马神经元凋亡的影响。方法取离体培养的大鼠海马神经元,随机分为4组:对照组 (A组)、二氮嗪30／μmol/L组(B组)、二氮嗪100 μmol/L组(C组)、二氮嗪100 μmol/L+Mito-KATP特异性阻断剂5-羟葵酸100μmol/L组(D组),各组神经元每天给予相应药物预处理1 h,连续3 d,继而缺氧4 h 复氧24 h,观察神经元的活力、凋亡率、Bax和Bcl-2蛋白的表达水平。结果与其它3组比较,C组海马神经元活力增强,凋亡率降低,Bcl-2蛋白表达水平升高,Bax蛋白表达水平下降(P<0．01)。结论 100μmol／L二氮嗪预处理通过改善Bcl-2与Bax蛋白表达的失衡,降低神经元的凋亡,对大鼠海马缺氧复氧神经元产生了保护效应。
Objective To investigate the effect of diazoxide preconditioning on mitochondrial ATP sensitive potassium channel (Mito-KATP) specific opener on hippocampal neuron apoptosis after hypoxia-reoxygenation. Methods Rat hippocampal neurons cultured in vitro were randomly divided into 4 groups: control group (group A), diazoxide 30 / μmol / L group (group B), diazoxide 100 μmol / L group ), Diazoxide 100 μmol / L + Mito-KATP specific inhibitor 5 μmol / L 100 μmol / L group (group D). Neurons in each group were pretreated with corresponding drugs for 1 h every day for 3 d After 4 hours of hypoxia reoxygenation for 24 hours, the neuron activity, apoptosis rate, Bax and Bcl-2 protein expression were observed. Results Compared with the other three groups, the activity of hippocampal neurons in C group was increased, the apoptosis rate was decreased, the expression of Bcl-2 protein and Bax protein were decreased (P <0.01). Conclusions 100μmol / L diazoxide preconditioning can protect rat hippocampus hypoxia-reoxygenated neurons by improving the imbalance of Bcl-2 and Bax protein expression and decreasing neuronal apoptosis.