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目的建立体外培养大鼠海马神经元糖氧剥夺/复氧轴突损伤模型。方法取体外培养7d的海马神经元,分为正常对照组和糖氧剥夺/复氧组。后者分别在糖氧剥夺0.5、1.0、1.5h再复糖复氧。常氧状态下检测各组复氧后1、5、24、48、72h培养液中的LDH活性,并观察神经元形态和轴突长度的变化。结果糖氧剥夺/复氧后的神经元折光性降低,胞体肿胀,并且轴突逐渐变短,同时LDH水平随时间延长增加。其中糖氧剥夺0.5h再复氧组效果最佳,其轴突缩短明显且神经元存活率较高。结论成功建立了体外培养SD大鼠海马神经元糖氧剥夺/复氧轴突损伤模型。
OBJECTIVE: To establish a rat model of in vitro cultured rat hippocampal neurons with glucose-oxygen deprivation / reoxygenation axon injury. Methods Hippocampal neurons cultured in vitro for 7 days were divided into normal control group and glucose-oxygen deprivation / reoxygenation group. The latter were deprived of glucose oxygen 0.5, 1.0, 1.5h and then re-sugar reoxygenation. Under normoxic condition, LDH activity in culture media was detected at 1, 5, 24, 48 and 72 h after reoxygenation in each group, and the changes of neuronal morphology and axon length were observed. Results After the oxygen-glucose deprivation / reoxygenation, the refolding of neurons decreased, the somatic cells swollen, and the axons became shorter and the level of LDH increased with time. Oxygen deprivation of oxygen 0.5h and reoxygenation group the best effect, its axons shortened significantly and higher survival rate of neurons. Conclusion SD rat hippocampal neurons were successfully established in glucose-oxygen deprivation / reoxygenation axonal injury model.