甲基乙二醛诱导大鼠海马神经元氧化应激损伤的实验研究-东南大学学报医学版

甲基乙二醛诱导大鼠海马神经元氧化应激损伤的实验研究

单位：东南大学,临床医学院,江苏,南京,210009

分类号：R-33, R651.15

出版年·卷·期（页码）：2008·27·第三期（212-216）

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24h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24h,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10mmol·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10mmol·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 MTT 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.

参考文献：

[1] GISPEN W H, BIESSELS G J. Cognition and synaptic plasticity in diabetes mellitus. 2000. doi:10.1016/S0166-2236(0)01656-8
[2] 秦锦标, 周红, 郑秀琴. 氟西汀对海马神经元生长的影响. 现代医学2007(4). doi:10.3969/j.issn.1671-7562.2007.04.005
[3] MOREIRA P I, SANTOS M S, SEICA R. Brain mitochondrial dysfunction as a link between Alzheimer's disease and diabetes. 2007. doi:10.1016/j.jns.2007.01.017
[4] STEEN E, TERRY B M, RIVERA E J. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease:is this type 3 diabetes?. 2005
[5] THORNALLEY P J. The glyoxalase system:new developments towards functional characterization of a metabolic pathway fundamental to biological life, 1990
[6] TUZCU M, BAYDAS G. Effect of melatonin and vitamin E on diabetes-induced learning and memory impairment in rats. 2006(1/3). doi:10.1016/j.ejphar.2006.03.024
[7] FUKUI K, ONODERA K, SHINKAI T. Impairment of learning and memory in rats caused by oxidative stress and aging,and changes in antioxidative defense systems, 2001
[8] FUKUI K, OMOI N O, HAYASAKA T. Cognitive impairment of rats caused by oxidative stress and aging,and its prevention by vitamin E, 2002
[9] LORETO S D, CARACCIOLO V, COLAFARINA S. Methylglyoxal induces oxidative stress-dependent cell injury and up-regulation of interleukin-1?and nerve growth factor in cultured hippocampal neuronal cells. 2004(2). doi:10.1016/j.brainres.2004.01.066
[10] LORETO S D, ZIMMITTI V, SEBASTIANA P. Methylglyoxal causes strong weakening of detoxifying capacity and apoptotic cell death in rat hippocampal neurons, 2008(2)

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