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采用MTT法和激光共聚焦显微术观察皮质酮对原代培养海马神经细胞的存活率及其线粒体膜电位的影响。结果表明 ,在低糖、无血清培养条件下 ,皮质酮可剂量依赖地降低海马神经元及神经胶质细胞的存活率 ,在同等剂量下以神经元损伤更为显著。给予高浓度葡萄糖 (2 5mmol/L)可明显拮抗皮质酮对海马神经元的毒性作用。进一步研究表明 ,皮质酮 (10 -6～ 10 -5mol/L)可引起海马神经元线粒体膜电位明显下降 ,此作用亦可被高浓度葡萄糖所对抗。结果提示 ,在相同处理因素条件下 ,皮质酮以损伤神经元为主。皮质酮可降低海马神经元的存活率及线粒体膜电位 ,给予高浓度葡萄糖具有明显地改善作用。线粒体膜电位的下降可能是皮质酮引起神经元损伤的机制之一。
The effects of corticosterone on the survival rate of primary cultured hippocampal neurons and mitochondrial membrane potential were observed by MTT and confocal microscopy. The results showed that under low glucose and serum-free culture conditions, corticosterone could reduce the survival rate of neurons and glial cells in a dose-dependent manner, and the neuron damage was more obvious under the same dose. Administration of high concentration glucose (25 mmol / L) significantly antagonized the neurotoxic effects of corticosterone on hippocampal neurons. Further studies show that corticosterone (10 -6 ~ 10 -5mol / L) can cause a significant decrease in mitochondrial membrane potential of hippocampal neurons, this effect can be confrontation with high concentrations of glucose. The results suggest that under the same conditions of treatment, corticosterone mainly damages neurons. Corticosterone can reduce the survival rate of hippocampal neurons and mitochondrial membrane potential, given high concentrations of glucose has significantly improved. Decreased mitochondrial membrane potential may be one of the mechanisms by which corticosterone causes neuronal damage.