中国现代医学杂志2018，Vol.28Issue(4)：1-5,5.DOI:10.3969/j.issn.1005-8982.2018.04.001
TAK-242对Aβ25-35诱导大鼠海马神经元损伤的作用及其机制研究
Effect of TAK-242 on β-amyloid peptide-induced neurotoxicity in hippocampi of rats and its mechanism
葛宇松 1马成永 1徐晏雯 1林永忠1
作者信息
- 1. 大连医科大学附属第二医院 神经内科,辽宁 大连 116023
- 折叠
摘要
Abstract
Objective To explore the effect of TAK-242 on β-amyloid peptide25-35 (Aβ25-35)-induced neural injury in rat hippocampi and the potential mechanism. Methods Aβ25-35 was injected into bilateral hippocampi of rats to build up Alzheimer's disease (AD) mode, then TAK-242 was injected to rat intraperitoneally. The morphological features and the amount of neurons in the CA3 area of hippocampi were observed after Nissl staining. The expressions of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) proteins were detected by Western blot. The levels of IL-1β and TNF-α were tested by ELISA. Results Injection of Aβ25-35 into hippocampi caused neuronal damage and loss in the CA3 area, however, TAK-242 could protect neurons in hippocampi against Aβ25-35-induced injury. Meanwhile, TAK-242 could reduce Aβ25-35-induced increase of TLR4, MyD88, IL-1β and TNF-α proteins. Conclusions TAK-242 could inhibit Aβ25-35-induced toxic role on neurons in the CA3 area of hippocampi through down-regulation of the TLR4/MyD88 signaling pathway and reduction of inflammatory factors IL-1β and TNF-α.关键词
阿尔茨海默病/β-淀粉样蛋白/TAK-242/Toll样受体4/髓样分化因子88Key words
Alzheimer's disease/amyloid beta-protein/TAK-242/Toll-like receptor 4/myeloid differentiation factor 88分类
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葛宇松,马成永,徐晏雯,林永忠..TAK-242对Aβ25-35诱导大鼠海马神经元损伤的作用及其机制研究[J].中国现代医学杂志,2018,28(4):1-5,5.
