溶血磷脂酸对THP-1细胞Toll样受体4/核因子-κB信号通路的影响  

The effect of lysophosphatidie acid on the expression of toll like receptor 4/nuclear factor kappaB signaling pathway in THP-1cell

作　　者：牛建平[1] 周志斌[2] 宋叶华[1] 林俊[1] 

机构地区：[1]厦门市第二医院神经内科,361021 [2]武汉科技大学附属天佑神经内科,430065

出　　处：《中华脑血管病杂志（电子版）》2013年第4期1-4,共4页Chinese Journal of Cerebrovascular Diseases(Electronic Edition)

基　　金：福建省自然科学基金(2010D010)

摘　　要：目的观察溶血磷脂酸（lysophosphatidieacid，LPA）对人单核细胞株THP-1细胞Toll-样受体4（tolllikereceptor4，TLR4）／核因子-κB（nuclearfactorkappaB，NF-κB）信号通路的影响，探讨LPA致动脉粥样硬化的机制。方法以不同浓度水平LPA（0～10μM）刺激人THP-1细胞4h，或以LPA1μM处理THP-1细胞不同时间（0-8h），荧光定量RT—PCR法测定TLR4mRNA表达，Westernblot检测TLR4蛋白、核蛋白NF-κBp65表达变化。结果IJPA以剂量依赖和时间依赖的方式上调THP-1细胞TLR4基因和蛋白的表达，并同步诱导THP-1细胞NF-κBp65活化。结论LPA可显著上调THP-1细胞TLR4表达及促进NF-κB的活化，LPA致粥样硬化作用可能部分是由TLR4／NF-κB信号途径介导的。Objectives expression of toll like receptor To study the effect of lysophosphatidie acid （LPA） on the 4/nuclear factor kappaB signaling pathway in THP-lcell line, and to further investigate the mechanism of atherosclerosis caused by LPA. Methodes Human THP-lcells were stimulated with LPA at different concentrations （ 0 - 10 pL M ） or at 1 I~ M for different time durations （0 - 8 h ） , TLR-4 mRNA and protein was measured by real-time RT- PCR and Westernblot respectively, the activity of NF-κB p65 subunit was detected by Westernblot according to the expression level of NF-κ B p65 protein in cell nucleus. Results LPA enhanced TLR-4 expression in mRNA, protein levels and the NF-κ B p65protein levels in cell nucleus. The enhancement effects occurred in concentration- and time-dependent manners. Conclusion LPA may synchronously increase the expression of TLR-4 and activate the NF- K B p65, the atherogenic effect of LPA maybe partially mediated through TLR4/N F-κB pathway.

关 键 词：溶血磷脂酸 THP-1细胞 TOLL样受体4 核因子-ΚB 

分 类 号：R363[医药卫生—病理学]