天然产物研究与开发 ›› 2018, Vol. 30 ›› Issue (3): 385-389.doi: 10.16333/j.1001-6880.2018.3.007

• 研究论文 • 上一篇    下一篇

Aβ1-42寡聚体通过PI3K-AKT信号通路诱导神经胶质细胞内TNF-α表达的机制研究

张海波1*,孙阳2   

  1. 1沈阳医学院附属中心医院神经外二科,沈阳 110024;2沈阳急救中心,沈阳 110000
  • 出版日期:2018-04-08 发布日期:2018-04-08

Aβ1-42  Oligomer Induces the Expression of TNF-α through PI3K-AKT Signaling Pathway in Neurogliocyte

ZHANG Hai-bo1*, SUN Yang2   

  1. 1The Second Department of Neurosurgery,the Affiliated Central Hospital of Shenyang Medical College,Shen Yang 110024,China; 2Shenyang First Aid Center,Shen Yang 110000,China  
  • Online:2018-04-08 Published:2018-04-08

摘要: 本文主要应用Western blot和Real-Time PCR等实验方法考察Aβ1-42寡聚体通过AKT信号通路对人源胶质母细胞瘤A172和鼠源胶质母细胞瘤D1A细胞中TNF-α表达的影响,同时应用免疫荧光的实验方法,进一步检测Aβ1-42寡聚体诱导TNF-α表达的具体调控机制。结果发现,A172和D1A细胞经Aβ1-42寡聚体处理后,Aβ1-42寡聚体可上调炎症因子TNF-α的表达,并且免疫荧光结果显示,此诱导作用是通过PI3K-AKT信号通路实现的。基于本实验研究,说明Aβ1-42寡聚体参与AD患者脑内炎症反应的发生,提示抗炎及抗Aβ形成在阿尔茨海默病的临床治疗方面具有重要的理论意义。

关键词: &beta, -淀粉样蛋白1-42, 肿瘤坏死因子-&alpha, 神经胶质细胞, AKT信号通路

Abstract: In this study,Western blot and Real-Time PCR methods were used to investigate the effects of Aβ1-42 oligomers on TNF-alpha expression in human glioblastoma A172 and murine glioblastoma D1A cells by AKT signaling pathway,at the same time,the specific regulation mechanism of Aβ1-42 oligomer induced TNF-alpha expression was detected by immunofluorescence assay.The results showed that Aβ1-42 oligomers can upregulate the expression of inflammatory factor TNF-alpha after treating A172 and D1A cells with Aβ1-42oligomers,and this induction is achieved via the PI3K-AKT signaling pathway.Based on this experimental study,we demonstrate that Aβ1-42oligomers participate in the inflammatory reaction in the AD brains,and suggest that anti-inflammation and anti Aβ have important theoretical significance in the clinical treatment of Alzheimer's disease.

Key words: Aβ1-42, TNF-α, Glial cells, AKT signaling pathway

中图分类号: 

R741.02