MnTDM阻断百草枯诱导的N27细胞生长抑制的作用  

Protective effects of SOD mimetic on N27 cell injury induced by Paraquat

作　　者：陈平[1] 汪世龙[1] 陈震[2] 李昂[1] 吴晓康[2] 赵春军[1] 梁立平[1] 

机构地区：[1]同济大学生命科学与技术学院,上海200092 [2]同济大学附属上海市第十人民医院脑外科,上海200072

出　　处：《第三军医大学学报》2007年第24期2343-2346,共4页Journal of Third Military Medical University

摘　　要：目的探讨在离体培养的细胞中,SOD类似物[manganese(Ⅲ)meso-tetrakis(N,N′-diethylimidazolium-2-yl)porphyrin,MnTDM]阻断百草枯诱导的N27细胞生长抑制作用。方法以N27细胞为多巴胺能神经元的细胞模型,检测不同浓度的MnTDM对百草枯诱导的N27细胞损伤的阻断作用,四甲基偶氮唑盐(MTT)法检测细胞活性及代谢状态,免疫细胞化学及Western blot检测酪氨酸羟化酶(tyrosine hydroxylase,TH)的表达,丙二醛(malondialdehyde,MDA)由硫代巴比妥酸(thiobarbituric acid,TBA)法测定。结果经百草枯作用后N27细胞活性下降,且其下降程度与百草枯浓度的升高呈线性关系。百草枯明显抑制N27细胞TH表达和明显升高MDA的浓度。MnTDM明显阻断百草枯诱导的细胞活性下降(P<0.05)、TH表达抑制和MDA含量升高(P<0.05),且该阻断作用与MnTDM的浓度有关。结论氧化应激在百草枯介导的多巴胺能神经元损伤中起了重要作用,MnTDM对百草枯介导的氧化应激损害有一定的防治作用。提示其可能对帕金森病患者的临床防治有一定作用。Objective To determine if manganese （Ⅲ） meso-tetrakis （ N, N′-diethylimidazolium-2-yl） porphyrin （MnTDM）, a SOD mimetic, prevents the neurotoxicity of Paraquat in the dopa＇ minergic neurons. Methods N27 cell, a dopaminergic neuron cell line, was used as cell model of Parkinson＇ s disease （PD） after Paraquat induction. After MnTDM intervention, the cell viability and metabolic state of Paraquat induced N27 cells were measured by MTT assay. Their protein expression of tyrosine hydroxylase （TH） was examined by immunocytochemistry and Western blot, and malondialdehyde （MDA） was detected with thiobarbituric acid （TBA） method. Results MnTDM significantly inhibited Paraquat-induced decreased cell viability and dopaminergic cell density depletion in N27 cell line in a dose-dependent manner. MnTDM also prevented the changes of TH expression and the increasing of MDA that were both caused by Paraquat. Conclusion Oxidative stress may play a role in the pathogenesis of Paraquat-induced dopaminergic cell damage. MnTDM prevents the neurotoxicity of Paraquat to some extent, suggesting the potential clinical therapy for PD.

关 键 词：帕金森病 百草枯 氧化应激 抗氧化剂 

分 类 号：R338.1[医药卫生—人体生理学] R595.405[医药卫生—基础医学]