摘要
目的:探讨甲基乙二醛对大鼠海马神经元的损伤作用及其可能机制。方法:取新生24 h的SD大鼠分离并培养其海马神经元,第7天予甲基乙二醛(MGO)或(和)N-乙酰半胱氨酸(NAC)干预24 h,四甲基偶氮唑蓝(MTT)法检测MGO或(和)NAC对海马神经元活力的影响,并以氧化敏感的2,7-二氢二氯荧光素(DCFH-DA)染色,荧光显微镜观察及流式细胞仪测定细胞内活性氧(ROS)强度。结果:MTT法检测结果显示,随MGO浓度增加,海马神经元存活率逐渐降低(均P<0.05),而NAC能显著增加海马神经元存活率,且10 mmol.L-1组存活率最高(P<0.01);100μmol.L-1MGO能使细胞内ROS水平明显增加(P<0.01),而同时加入10 mmol.L-1NAC能够抑制MGO导致的细胞内ROS增高。结论:MGO可能部分通过诱导细胞内ROS产生,导致神经元氧化应激损伤,而NAC可能通过降低ROS的水平而对神经元起保护作用。
Objective To investigate the effect of methylglyoxal（MGO） on hippocampal neuronal cells and to discuss the possible mechanism. Methods Primary cultures of 1-day-old SD rat hippocampal neurons were exposed to MGO and（or） N-acetyl-l-cysteine （NAC） for 24 h respectively. Cell viability was assessed by the MTr assay. Cells were marked with oxidation-susceptible fluroscent probe 2,7-dichorofluoresin diacetate（DCFH） ,and mean fluroscent intensity （MFI） was assayed by flow cytometry. Results The rate of survived cells in the MGO groups was lower than that of the control group. MGO increased the concentration of reactive oxygenspecies （ROS） in the hippocampal neurons, and the effects of MGO on hippocampal neuron could be ameliorated by NAC. Conclusion The induction of ROS in hippocampal neurons by MGO may play an important role in oxidative stress-dependent cell injury and NAC can protect hippocampal neurons by decreasing the ROS level.
出处
《东南大学学报（医学版）》
CAS
2008年第3期212-216,共5页
Journal of Southeast University(Medical Science Edition)
