丹参酮ⅡA对EA.hy926细胞TLR4/NF-κB炎症信号通路的影响  

Effect of tanshinone ⅡA on TLR4 /NF-κB signal pathway of endothelial cells

作　　者：贾连群[1] 冯峻屹[1] 杨关林[1] 刘春英[1] 曹阳[1] 张林[1] 

机构地区：[1]辽宁中医药大学,沈阳辽宁110032

出　　处：《中国生化药物杂志》2011年第5期337-340,共4页Chinese Journal of Biochemical Pharmaceutics

基　　金：中国博士后科学基金项目(20090451279);辽宁省教育厅创新团队基金项目(2009T068);辽宁省科技厅博士启动基金项目(20091052);辽宁中医药大学博士启动基金

摘　　要：目的观察丹参酮ⅡA对脂多糖(LPS)诱导人脐静脉细胞融合细胞EA.hy926 TLR4/NF-κB炎症信号通路的影响,探讨丹参酮ⅡA抗动脉粥样硬化(AS)的作用机制。方法体外培养人脐静脉细胞融合细胞EA.hy926;观察丹参酮ⅡA低、中、高剂量组对LPS刺激EA.hy926细胞的保护作用,RT-PCR和Western bolt法检测TLR4、NF-κB、TNF-αmRNA和蛋白表达。结果 LPS刺激组TLR4、NF-κB和TNF-αmRNA和蛋白表达较正常组明显增加(P<0.05)。与LPS刺激组相比,丹参酮ⅡA低剂量组TLR4、NF-κB、TNF-αmRNA及蛋白表达无明显差异,而丹参酮ⅡA中、高剂量组TLR4、NF-κB和TNF-αmRNA及蛋白质表达明显降低(P<0.05)。结论丹参酮ⅡA抗AS的作用机制之一是通过干预TLR4/NF-κB信号通路来实现的。Purpose To observe the influence of tanshinone ⅡA on the TLR4 /NF-κB inflammatory signal pathway in cultured human umbilical veins endothelial cells EA.hy926 induced by LPS,and to in-vestigate the molecular mechanism of tanshinone ⅡA against atherosclerosis（AS）.Methods The human cells EA.hy926 were cultured in vitro.Observing the effect of low,middle,high dose of tanshinone ⅡA on EA.hy926 stimulated by LPS.The mRNA and protein expression of TLR4,NF-κB and TNF-α were tested by RT-PCR and Western blot method respectively.Results The mRNA and protein expression of TLR4、NF-κB and TNF-α were promoted significantly（P〈0.05）.Low dose of tanshinone ⅡA has no ob-vious difference of the expression from those of LPS stimulating group.However,middle and high dose of tanshinoneⅡ A could obviously inhibit the expression of TLR4,NF-κB and TNF-α（P〈0.05）.Conclu-sion One of the molecular mechanisms of tanshinone ⅡA against AS is to intervene the TLR4 /NF-κB in-flammatory signal pathway.

关 键 词：丹参酮ⅡA 动脉粥样硬化 炎症 信号通路 

分 类 号：R392.11[医药卫生—免疫学] R966[医药卫生—基础医学]