摘要
目的:探讨氧自由基在阿尔茨海默病(AlzheimerDisease熏AD)发生中的作用及可能机制,评价褪黑素(Melatonin熏MT)的临床应用价值。方法:采用超氧自由基产生系统黄嘌呤/黄嘌呤氧化酶系统(X/XO)作用于PC12细胞,以褪黑素拮抗其作用,观察细胞的形态学变化;MTT法检测细胞存活率,DNA电泳和流式细胞术分析细胞凋亡情况,RT鄄PCR技术测定凋亡相关基因bcl鄄2、bax的表达。结果:X/XO作用后,PC12细胞出现凋亡特征性改变,凋亡率增加,电泳呈现DNAladders,凋亡相关基因bax上调;而10-5M褪黑素即能改善凋亡情况。结论:氧自由基可诱导神经元凋亡从而促进AD发生,其机制与促凋亡相关基因Bax表达增高有关;褪黑素可减缓神经元凋亡,可用于临床预防与治疗。
Objective: To observe the toxic effects of reactive oxygen species(ROS) on neurons and study the mechanism by which neurotoxins lead to Alzheimer Disease and evaluate the therapeutic value of Melatonin. Methods: After treating PC12 cells with X/XO in one group and adding Melatonin in another group, we measured the changes of apoptotic cells by electron microscope, MTT assay, DNA electrophoretic analysis, and flow cytometric analysis. Apoptosis-associated gene (AAG) bax and bcl-2 in cells were detected by reverse transcription-PCR. Results: Exposure of cells to X/XO resulted in characteristic DNA fragmentation and an increase in the apoptosis rate, as well as an elevation of bax. NO obvious hallmarks of apoptosis were found in Melatonin(10-5M) group. Conclusion: ROS can induce neuron apoptosis whose mechanism may relate to AAG; Melatonin can protect neurons against ROS-induced apoptosis.
出处
《山东大学学报（医学版）》
CAS
2004年第6期629-632,共4页
Journal of Shandong University:Health Sciences
关键词
活性氧
阿尔茨海默病
细胞凋亡
Reactive oxygen species
Alzheimer disease
Apoptosis
