谷氨酸致原代培养皮层神经元损伤中自噬的激活  

Autophagy is activated during glutamic acid-induced cortical neuron injury

作　　者：陈兆耀[1] 陈茂刚[1] 卢婷婷[1] 倪冠中[1] 刘新峰[1] 徐格林[1] 

机构地区：[1]南京大学医学院临床学院,南京军区南京总医院神经内科,江苏南京210002

出　　处：《中国病理生理杂志》2011年第1期62-66,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30870848)

摘　　要：目的:体外观察谷氨酸介导的神经元氧化性损伤中自噬的激活,以及抑制自噬对谷氨酸致神经元毒性损伤的保护作用。方法:体外培养皮层神经元,给予谷氨酸以及自噬抑制剂3-甲基腺嘌呤干预,MTT法检测细胞活力,透射电镜观察自噬泡的产生,激光共聚焦显微镜观察自噬特异性蛋白LC3的表达。结果:给予谷氨酸干预后皮层神经元细胞存活率下降,自噬体数目明显增加,自噬标志性蛋白LC3表达增加。给予3-甲基腺嘌呤后,神经元细胞存活率增加,细胞自噬水平下降。结论:谷氨酸诱导的神经元毒性损伤中存在自噬相关性细胞死亡,抑制自噬可能对谷氨酸毒性损伤有抑制作用,自噬抑制剂3-甲基腺嘌呤具有一定的神经保护作用。AIM：To investigate whether autophagy is activated during glutamic acid-induced neuron injury and the possible neuroprotective effect of 3-methyl adenine（3-MA）（an autophagy inhibitor）.METHODS：Glutamic acid or 3-MA was added to the medium of cultured cortical neurons.Cell viability was measured by MTT assay.The formation of autophagosome was observed under transmission electron microscope.The marker protein light chain 3（LC3） for autophagy was detected by immunofluorescence assay and visualized under laser confocal microscope.RESULTS：The cell viability declined during glutamic acid treatment and the autophagosomes were increased.LC3,the marker protein of autophagy,also significantly increased.The autophagy level was lowered by 3-MA,and cell viability was increased.CONCLUSION：The results suggest that autophagy is activated during glutamic acid treatment and inhibition of autophagy may have neuroprotective effect.The autophagy inhibitor 3-MA may be a potential neuroprotective agent.

关 键 词：自吞噬作用 3-甲基腺嘌呤 神经元 谷氨酸 

分 类 号：R363[医药卫生—病理学]