淫羊藿苷对脂多糖诱导人脐静脉内皮细胞炎症因子表达的影响及机制研究  

Effects of icariin on secretion of inflammatory cytokines in human umbilical vein endothelial cells induced by lipopolysaccharide

作　　者：吴迪[1] 杨滔 杜清 Wu Di, Yang Tao, Du Qing(Teaching Demonstration Center of Pharmaceutical Experiment, School of Pharmacy, Zunyi Medical University, Zunyi Guizhou 563099, Chin)

机构地区：[1]遵义医学院药学院药学实验教学示范中心,贵州遵义563099

出　　处：《遵义医学院学报》2018年第1期20-25,共6页Journal of Zunyi Medical University

基　　金：遵义医学院硕士启动基金资助项目(NO:F-669)

摘　　要：目的探讨淫羊藿苷对脂多糖诱导人脐静脉内皮细胞分泌炎症因子的影响,并探讨其作用机制。方法体外培养人脐静脉内皮细胞并鉴定,实验分为4组:空白组、脂多糖模型组、淫羊藿苷(1、10、50μmol/L)实验组和机制研究组。采用MTT法检测人脐静脉内皮细胞活力,Western-blot法检测TLR4及NF-κB蛋白水平,ELISA试剂盒测定细胞上清液C-反应蛋白(CRP)、白细胞介素6(IL-6)蛋白表达水平。结果与空白组相比,脂多糖模型组CRP、IL-6、TLR4及NF-κB蛋白水平显著升高,有统计学差异(P<0.05)。与脂多糖模型组对比,淫羊藿苷实验组CRP、IL-6、TLR4及NF-κB蛋白水平显著降低,有统计学差异(P<0.05),并呈一定的浓度依赖性。加入TLR4阻断剂后,机制研究组CRP、IL-6、TLR4及NF-κB蛋白表达较模型组显著降低,有统计学差异(P<0.05),但蛋白水平表达的抑制作用不如高剂量淫羊藿苷组(50μmol/L)。结论淫羊藿苷对脂多糖诱导的人脐静脉内皮细胞炎症损伤具有一定的保护作用,其作用与抑制TLR4诱导的NF-κB信号通路,下调下游炎症因子CRP、IL-6的释放有关。Objective To investigate the effects and mechanism of icariin（ ICA） on secretion of inflammatory cytokines in human umbilical vein endothelial cells（ HUVECs） caused by lipopolysaccharide（ LPS）. Methods HUVECs were cultured and identified in vitro,and then divided into four groups： blank group,model group,experimental group and mechanism group. The cell viability was determined by MTT assay,the levels of TLR4 and NF-κB protein were measured by Western-blot,and the CRP and IL-6 protein expression were measured by ELISA. Results Compared with the control group,the levels of CRP,IL-6,TLR4 and NF-κB protein were significantly increased（ P〈0. 05） in the model group. Compared with the model group,the levels of CRP,IL-6,TLR4 and NF-κB protein were significantly reduced（ P〈0. 05） in the experimental group with a dose-dependent manner. Adding TLR4 inhibitor,the levels of CRP,IL-6,TLR4 and NF-κB protein were significantly lower than that of the model group（ P〈0. 05）,but the inhibition effect on protein expression was weaker than that of the experimental group（ high dose,50 μmol/L）. Conclusion ICA could protect HUVECs from LPS-induced injury. The action mechanisms of ICA may be related to the inhibition of HUVECs inflammation through TLR4/NF-κB signaling pathway.

关 键 词：淫羊藿苷 脂多糖 人脐静脉内皮细胞 炎症因子 

分 类 号：R972[医药卫生—药品]