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用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理小鼠后黑质中bax表达增加。

Increase in bax expression in substantia nigra following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of mice.

作者信息

Hassouna I, Wickert H, Zimmermann M, Gillardon F

机构信息

Physiologisches Institut, Universitat Heidelberg, Germany.

出版信息

Neurosci Lett. 1996 Feb 2;204(1-2):85-8. doi: 10.1016/0304-3940(96)12323-5.

Abstract

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mammals causes damage to the nigrostriatal pathway similar to that observed in Parkinson's disease. In the present study, we have investigated alterations in cell death effector gene expression induced by the neurotoxin MPTP in mouse substantia nigra. Intraperitoneal MPTP injections in mice resulted in a significant increase in bax mRNA by about two- and three-fold after 3 and 6 days, respectively. The up-regulation of bax mRNA was associated with concomitant increase in Bax immunoreactivity observed mainly in large- and medium-sized neurons in the substantia nigra that are destined to die. Our results indicate a pathophysiological significance of bax, which promotes programmed cell death, in MPTP neurotoxicity.

摘要

给哺乳动物注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)会导致黑质纹状体通路受损,这与帕金森病中观察到的情况相似。在本研究中,我们调查了神经毒素MPTP诱导的小鼠黑质中细胞死亡效应基因表达的变化。给小鼠腹腔注射MPTP后,分别在3天和6天后,bax mRNA显著增加了约两倍和三倍。bax mRNA的上调与Bax免疫反应性的相应增加相关,主要在黑质中注定死亡的大、中型神经元中观察到。我们的结果表明,促进程序性细胞死亡的bax在MPTP神经毒性中具有病理生理学意义。

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