Aβ_(1-42)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

Aβ_(1-42) Oligomer Induces the Expression of TNF-αthrough PI3K-AKT Signaling Pathway in Neurogliocyte

本文主要应用Western blot和Real-Time PCR等实验方法考察Aβ_(1-42)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Aβ_(1-42)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Aβ_(1-42)寡聚体处理后,Aβ_(1-42)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Aβ_(1-42)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。

In this study,Western blot and Real-Time PCR methods were used to investigate the effects of A beta 1-42 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 Aβ-1-42 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 Aβ1-42 oligomers,and this induction is achieved via the PI3K-AKT signaling pathway.Based on this experimental study,we demonstrate that Aβ1-42 oligomers participate in the inflammatory reaction in the AD brains,and suggest that anti-inflammation and anti Aβhave important theoretical significance in the clinical treatment of Alzheimer's disease.