T-588对培养神经元中血清剥夺和β-淀粉样蛋白所致毒性损伤的保护作用。

Protective effect of T-588 on toxic damage by serum deprivation and amyloid-beta protein in cultured neurons.

作者信息

Yamamuro Akiko, Ago Yukio, Maeda Sadaaki, Sakai Yoshiyuki, Baba Akemichi, Matsuda Toshio

机构信息

Laboratory of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University.

出版信息

J Pharmacol Sci. 2003 Jun;92(2):153-6. doi: 10.1254/jphs.92.153.

DOI:10.1254/jphs.92.153

PMID:12832844

Abstract

The present study examines the effect of the cognition enhancer (1R)-1-benzo[b]thiophen-5-yl-2-[2-(diethylamino)ethoxy]ethan-1-ol hydrochloride (T-588) on neuronal injury induced by serum deprivation or amyloid-beta protein (A beta). T-588 protected partially against neuronal injury induced by serum deprivation or A beta in cultured cortical neurons. T-588 did not affect the phosphorylation of extracellular signal-regulated kinase (ERK) in cortical neurons and SH-SY5Y cells. These results suggest that T-588 has a protective effect in neuronal injury models and the effect is not mediated by an ERK signal pathway.

摘要

本研究考察了认知增强剂（1R）-1-苯并[b]噻吩-5-基-2-[2-（二乙氨基）乙氧基]乙醇盐酸盐（T-588）对血清剥夺或β-淀粉样蛋白（Aβ）诱导的神经元损伤的影响。T-588对培养的皮质神经元中血清剥夺或Aβ诱导的神经元损伤具有部分保护作用。T-588不影响皮质神经元和SH-SY5Y细胞中细胞外信号调节激酶（ERK）的磷酸化。这些结果表明，T-588在神经元损伤模型中具有保护作用，且该作用不是由ERK信号通路介导的。