摘要
目的探讨氧化应激在鱼藤酮多巴胺能神经元PC12细胞中的毒性作用。方法用高分化的PC12细胞作为多巴胺能神经元的细胞模型,经不同浓度的鱼藤酮处理,观察细胞形态及其超微结构,四甲基偶氮唑盐法检测细胞活性和增殖抑制及细胞代谢状态,生化分析法检测SOD活力、MDA含量,特异性DCF-DA荧光探针检测细胞内ROS水平。结果经鱼藤酮处理24 h后PC12细胞突起样结构消失,细胞体积变小、形态变圆,部分细胞呈悬浮状态;细胞线粒体代谢和超微结构发生改变;PC12细胞增殖抑制,细胞活性降低;细胞内的SOD活力下降,MDA含量增高;荧光探针标记显示PC12细胞荧光强度增加,细胞内ROS含量增加。结论鱼藤酮在体外对多巴胺能神经元有毒性作用,可抑制细胞增殖,影响线粒体代谢,氧化应激可能在鱼藤酮的多巴胺神经元毒性机制中起作用。
Objective To investigate the mechanism of oxidative stress in rotenone neurotoxicity onto dopaminergic neuron. Methods High differentiated PC12 cells as dopaminergic neurons were treated by different concentrations of rotenone. Cell morphology was observed with inverted phase contrast microscope and transmission electron microscope. SOD and MDA were detected with biochemical assay. And the specific fluorescent probe （DCF-DA） was used to examine the ROS in PC12 cells. Results After being treated with rotenone for 24 hours, most of PC12 cells treated by rotenone became smaller and rounder. The structure and metabolism of mitochondrial changed. Cell proliferation inhibition increased and cell activity decreased significantly when treated by rotenone. SOD increased and MDA decreased. The intensity of fluorescence was more obvious in PC12 cells treated by rotenone compared with control group. Conclusions In vitro, rotenone should be neurotoxic to dopaminergic neuron, It was suggested that rotenone might affect the metabolism of oxidative stress in the pathogenesis of dopaminergie neuron.
出处
《疾病控制杂志》
2006年第3期241-244,共4页
Chinese Journal of Disease Control and Prevention
基金
国家自然科学基金项目(30400347)
