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首页> 外文期刊>Neuropharmacology >A neuroprotective agent, T-817MA (1-{3-(2-(1-benzothiophen-5-yl)ethoxy)propyl} azetidin-3-ol maleate), prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity in mice.
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A neuroprotective agent, T-817MA (1-{3-(2-(1-benzothiophen-5-yl)ethoxy)propyl} azetidin-3-ol maleate), prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity in mice.

机译：一种神经保护剂T-817MA（1- {3-（2-（1-（1-苯并噻吩-5-基）乙氧基）丙基}氮杂环丁烷-3-醇马来酸酯）可以预防1-甲基-4-苯基-1,2 3，6-四氢吡啶诱导的小鼠神经毒性。

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摘要

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.
机译：T-817MA（1- {3- [2-（1-苯并噻吩-5-基）乙氧基]丙基}马来酸酯氮杂环丁烷-3-醇）是阿尔茨海默氏病的候选治疗药物，可抑制氧化应激和一氧化氮诱导的神经毒性并作为神经营养因子。本研究检查了T-817MA对C57BL / 6J小鼠中1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的多巴胺能神经毒性的影响。 MPTP处理（10mg / kg，每2小时间隔s.c.x4）损害了旋转脚架性能，T-817MA改善了这一缺陷。 MPTP处理还降低了黑质（SNc）和纹状体中的多巴胺水平和酪氨酸羟化酶免疫染色。用T-817MA（10和30mg / kg，如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下降，但不影响脑中1-MP-4-苯基吡啶鎓离子（MPTP的活性代谢产物）的水平。 。 SNc中的保护作用几乎完全，但纹状体中仅部分。 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，而T-817MA可能会阻断它。 MPTP引起SNc和纹状体中的小胶质细胞活化，但是T-817MA并不影响小胶质细胞的活化。这些结果表明，T-817MA可通过阻止SNc中的脂质过氧化来防止MPTP诱导的神经毒性，并暗示该化合物可用于治疗与氧化应激相关的神经退行性疾病，例如帕金森氏病。

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