Tsao L I, Su T P
Cellular Pathobiology Unit, Cellular Neurobiology Research Branch, National Institute on Drug Abuse, NIH, Baltimore, MD 21224, USA.
Eur J Pharmacol. 2001 Sep 28;428(1):149-51. doi: 10.1016/s0014-2999(01)01346-2.
The psychostimulant methamphetamine, both in vivo and in vitro, caused a mitochondrial cytochrome c release, the translocation of Bax from cytosol into mitochondrion, and the oligomerization of Bax. These effects by methamphetamine were blocked by a neuroprotective and hibernation-induction delta opioid peptide [D-Ala2,D-Leu5]enkephalin (DADLE). These results suggest that methamphetamine causes apoptosis by affecting the dynamics of Bax and that the neuroprotective property of DADLE may be due partly to its ability to potently block Bax-related apoptotic processes.
精神兴奋剂甲基苯丙胺在体内和体外均会导致线粒体细胞色素c释放、Bax从胞质溶胶转位至线粒体以及Bax寡聚化。甲基苯丙胺的这些作用可被具有神经保护和诱导冬眠作用的δ阿片肽[D - Ala2，D - Leu5]脑啡肽（DADLE）阻断。这些结果表明，甲基苯丙胺通过影响Bax的动力学导致细胞凋亡，并且DADLE的神经保护特性可能部分归因于其有效阻断与Bax相关的凋亡过程的能力。
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