Investigations on methamphetamine-neurotoxicity by using an animal model

这项研究表明，考虑到甲基苯丙胺（METH）由于氧化应激引起的神经毒性作用，对NO合酶的药理学干预可能有助于减少甲基苯丙胺的单胺消耗和凋亡诱导作用，并且低剂量METH预处理可能对中脑的METH神经毒性具有保护作用，从而抑制氧化应激和凋亡机制，部分通过内质网应激相关通路。从法医病理学的角度来看，在神经毒性剂量给药前先给予低剂量METH的动物模型可用于研究METH滥用者的神经毒性机制。

This study suggests that, in consideration of the neurotoxic effects of methamphetamine(METH) due to oxidative stress, pharmacological intervention on NO synthase may help reduce the monoamine-depleting and apoptosis-inducing effects of methamphetamine and that pretreatment with low-dose METH may be protective against METH neurotoxicity in the midbrain, leading to the suppression of oxidative stress and apoptotic mechanisms, in part via ER stress-related pathways. In the point of view of forensic pathology, an animal model of escalation drug intake and pretraetment of low-dose METH prior to neurotoxic-dose admistration could be useful to investigate the mechanisms involved in neurotoxicity of human METH abusers.