期刊文献+

还原型谷胱甘肽对MPTP损伤小鼠保护作用研究

Study on protective effects of the reduced glutathione pretreatment on MPTP toxicity to mice
暂未订购
导出
摘要 目的观察还原型谷胱甘肽(GSH)对1甲基4苯基1,2,3,6四氢吡啶(MPTP)损伤的小鼠黑质多巴胺神经元的影响及可能的作用机制。方法雄性C57BL小鼠给予还原型谷胱甘肽300mg/(kg·d)腹腔注射连用10天,第6天预防组另于皮下注射MPTP40mg/(kg·d),再应用5天,其间观察小鼠行为学变化;应用免疫细胞化学染色法观察黑质区酪氨酸羟化酶(TH)阳性神经元及活化型caspase3阳性细胞的变化。结果还原型谷胱甘肽可以抑制小鼠的黑质酪氨酸羟化酶阳性神经元减少及活化型caspase3阳性细胞激活。结论还原型谷胱甘肽可能对MPTP损伤的黑质多巴胺神经元凋亡有抗氧化保护作用。 Objective To observe the effect of reduced glutathione on dopamineric neurons in the substantia nigra in mice with a 1 methy 4 phenyl 1,2,3,6 tetrahydropyridine(MPTP) lesion and to study its possible mechanism.Methods C57BL mice were administrated i.h.with MPTP (40mg/kg·d) in 5 days to produce PD mouse model.Reduced glutathione (300mg/kg·d) were given i.p.5 days prior to MPTP in preventive groups and used consecutively for 10 days.Meanwhile,observed the varities of mouse behavior.Immunocytochemistry staining was used to detect Tyrosine hydroxylase (TH) and activation of caspase 3 positive cells.Results Pretreatment with reduced glutathione could prevent the loss of TH positive neurons and decrease the number of activation of caspase 3 positive cells.Conclusion Reduced glutathione may have protective effect on apoptosis and oxidative stress of substantia nigra neurons in MPTP induced PD mouse model.
出处 《哈尔滨医科大学学报》 CAS 北大核心 2005年第3期256-258,F004,共4页 Journal of Harbin Medical University
关键词 帕金森病 谷胱甘肽 MPIP 黑质多巴胺神经元 凋亡 Parkinson disease glutathione MPTP nigral dopaminergic neuron apoptosis
  • 相关文献

参考文献10

  • 1Jenner P.Oxidative stress in Parkinson's disease[J].Ann Neurol,2 003,53 (Suppl 3):S26-36.
  • 2杨宏彦,王晓民.帕金森病动物模型:揭开人类帕金森病奥秘的钥匙[J].生命科学,2002,14(5):275-278. 被引量:3
  • 3Sian J,Dexter DT,Lees AJ,et al.Alteration in glutathione levels in Parkinson's disease and other neurodegenerative disorders affecting basalg anglia[J].Ann Neurol,1994,36(3):348-355.
  • 4Mytilineou C,Kramer BC,Yabut JA.Glutathione depletion and oxidative stress[J].Parkinsonism Relat Disord,2002,8(6):385-387.
  • 5Paolicchi A,Dominici S,Pieri L,et al.Glutathione catabolism as asignaling mechanism[J].Biochem Pharmacol,2002,64(5-6):1027-1035.
  • 6Gohen GM.Caspase:the executioners of apoptosis[J].J Biochem,1997 ,326(1):1-16.
  • 7Turmel H,Hartmann A,Parain K,et al.Caspase-3 activaton in 1- methy1-1,2,3,6-tetrahydropyridine(MPTP)-treated mice[J].Mov Disord,2001,16( 2):185-189.
  • 8Bilsland J,Roy S,Xanthoudakis S,et al.Caspase inhibitors attenuate 1-methy1-4-phenylpyridinium toxicity in primary cultures of mesencephalic dopaminergic neurons[J].J Neurosci,2002,22(7):2637-2649.
  • 9陆建明,周厚广,鲍远程.还原型谷胱甘肽对左旋多巴毒性拮抗作用的实验研究[J].中国临床神经科学,2004,12(1):36-38. 被引量:4
  • 10Fitzmaurice PS,Ang L,Guttman M,et al,Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease[J].Mov Disord,2003,18 (9):969-976.

二级参考文献19

  • 1[1]Blum D, Torch S, Lambeng N, et al. Prog Neurobiology, 2001; 65: 135-172.
  • 2[2]Beal M F. Nature Rev Neurosci, 2001; 2: 325-332.
  • 3[3]Crocker S J, Wigle N, Liston P, et al. Eur J Neurosci,2001; 14: 391-400.
  • 4[4]Reed J C. Trends Mol Med, 2001; 7: 314-319.
  • 5[5]Teismann P, Ferger B. Synapse, 2001; 39: 167-174.
  • 6[6]Costantini L C, Douglas C, Pravin C, et al. Eur J Neurosci, 2001; 13: 1085-1092.
  • 7[7]Akerud P, Josep M C, Evan Y S, et al. J Neurosci,2001; 21: 8108-8118.
  • 8[8]Feany M B, Bender W W. Nature, 2000; 404: 394-398.
  • 9[9]Vila M, Wu D C, Przedborski S. Trends in Neurosci,2001; 24(Suppl): S49--S55.
  • 10[10]Zhang J, Graham D G, Montine T J, et al. J Neuropathol Exp Neurol, 2000; 59: 53-61.

共引文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部