氯通道电流在离体大鼠海马缺血缺氧性神经元凋亡中的变化及SITS的拮抗作用

Changes of chloride channel currents during cultured rat hippocampal neuronal apoptosis and anti-effects of SITS

目的:观察氯通道电流在NO诱导大鼠海马神经元损伤中的变化。方法:离体培养12d的SD大鼠海马神经元,随机分为正常对照组、SIN-1处理组和SIN-1处理后加氯通道阻断剂SITS组,观察细胞凋亡情况,全细胞膜片钳技术记录神经元氯通道电流。结果:3组神经元凋亡率比较,差异有统计学意义(F=3.120,P=0.006)。NO处理后的神经元氯通道电流增加;SITS能部分抑制神经元损伤后氯通道电流的增加。结论:氯通道可能参与了NO诱导的离体海马神经元损伤。

Aim：To observe the changes of chloride channel currents after neuronal injury induced by NO.Methods：Rat hippocampal neurons cultured for 12 days were randomly divided into normal control group,NO treatment group and NO treatment plus SITS group.The neuronal apoptosis of 3 groups was observed with MTT.The chloride channel currents were recorded with whole-cell mode of voltage clamp.Results：There was significant difference in neuronal apoptosis rate among the 3 groups（F=3.120,P=0.006）.The chloride channel currents in neurons exposed to NO were increased.SITS,one kind of chloride channel blocker,could partly decrease the increased currents.Conclusion： The chloride channels maybe participate in the neuronal injury following cerebral ischemia.