Kawasaki Toshiyuki, Ago Yukio, Kitao Tatsuya, Nashida Tetsuaki, Takagi Akiko, Takuma Kazuhiro, Matsuda Toshio
Laboratory of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka 565-0871, Japan.
Neuropharmacology. 2008 Oct;55(5):654-60. doi: 10.1016/j.neuropharm.2008.05.032. Epub 2008 Jun 5.
T-817MA (1-{3-[2-(1-benzothiophen-5-yl)ethoxy]propyl} azetidin-3-ol maleate) is a candidate therapeutic agent for Alzheimer's disease that inhibits oxidative stress and nitric oxide-induced neurotoxicity and acts as a neurotrophic factor. The present study examines the effect of T-817MA on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity in C57BL/6J mice. MPTP treatment (10mg/kg, s.c.x4 at 2-h intervals) impaired rotarod performance, and T-817MA improved this deficit. MPTP treatment also decreased dopamine levels and tyrosine hydroxylase immunostaining in the substantia nigra (SNc) and striatum. Pretreatment with T-817MA (10 and 30mg/kg as T-817, p.o.) attenuated these decreases in dopamine levels and tyrosine hydroxylase immunoreactivity, but did not affect brain levels of 1-methyl-4-phenylpyridinium ion, an active metabolite of MPTP. The protective effect was almost complete in the SNc, but only partial in the striatum. MPTP increased levels of the lipid peroxidation product, thiobarbituric acid reactive substance, only in the midbrain, which could be blocked by T-817MA. MPTP caused microglial activation both in the SNc and striatum, but T-817MA did not affect the activation of microglia. These results suggest that T-817MA protects against MPTP-induced neurotoxicity by blocking lipid peroxidation in the SNc, and imply that this compound may be useful for treating neurodegenerative disorders related to oxidative stress, such as Parkinson's disease.
T - 817MA(1 - {3 - [2 - (1 - 苯并噻吩 - 5 - 基)乙氧基]丙基}氮杂环丁烷 - 3 - 醇马来酸盐)是一种用于治疗阿尔茨海默病的候选治疗剂,它能抑制氧化应激和一氧化氮诱导的神经毒性,并作为一种神经营养因子发挥作用。本研究考察了T - 817MA对1 - 甲基 - 4 - 苯基 - 1,2,3,6 - 四氢吡啶(MPTP)诱导的C57BL/6J小鼠多巴胺能神经毒性的影响。MPTP处理(10mg/kg,皮下注射,间隔2小时共4次)损害了转棒试验表现,而T - 817MA改善了这一缺陷。MPTP处理还降低了黑质致密部(SNc)和纹状体中的多巴胺水平以及酪氨酸羟化酶免疫染色。用T - 817MA(10mg/kg和30mg/kg作为T - 817,口服)预处理可减轻多巴胺水平和酪氨酸羟化酶免疫反应性的降低,但不影响MPTP的活性代谢产物1 - 甲基 - 4 - 苯基吡啶离子的脑内水平。保护作用在SNc中几乎是完全的,但在纹状体中只是部分的。MPTP仅在中脑增加了脂质过氧化产物硫代巴比妥酸反应性物质的水平,这可被T - 817MA阻断。MPTP在SNc和纹状体中均引起小胶质细胞活化,但T - 817MA不影响小胶质细胞的活化。这些结果表明,T - 817MA通过阻断SNc中的脂质过氧化来保护小鼠免受MPTP诱导的神经毒性,并暗示该化合物可能对治疗与氧化应激相关的神经退行性疾病(如帕金森病)有用。