黄芪甲苷通过Toll-like受体通路对HepG2高脂细胞脂质积累的抑制作用  

Inhibitory effect of astragaloside on lipid accumulation in HepG2 cells via Toll-like receptor pathway

作　　者：杨柳[1] 熊小平 马国斌 李昱[1] 胡林[1] 丁海强 曾圣强 王洪[1] YANG Liu;XIONG Xiao-ping;MA Guo-bin(First Affiliated Hospital of Nanchang Medical College,Jiangxi Provincial People's Hospital,Nanchang 330006,China)

机构地区：[1]江西省人民医院(南昌医学院第一附属医院),330006 [2]江西省南昌市安义县人民医院,330003 [3]江西省南昌市进贤县人民医院,330000

出　　处：《中国现代药物应用》2022年第22期184-189,共6页Chinese Journal of Modern Drug Application

基　　金：江西省中医药科技计划项目(项目编号:2019A162);南昌医学院第一附属医院江西省人民医院博士启动基金(项目编号:19-236)。

摘　　要：目的探讨黄芪甲苷(AS-Ⅳ)对HepG2高脂细胞模型血脂代谢的影响以及Toll-like信号通路在其中的作用。方法使用HepG2细胞构建高脂血症模型,并随机分为六组:AS-Ⅳ低、中、高(0.05、0.1、0.2 mmol/L)剂量组,对照组,抑制剂组,AS-Ⅳ+抑制剂组。分别进行实时荧光定量聚合酶链式反应(PCR)和蛋白质免疫印迹(WB)分析,检测Toll样受体4(TLR4)、髓样分化因子88(MyD88)、肿瘤坏死因子受体相关因子6(TRAF6)mRNA和蛋白表达。结果①在AS-Ⅳ高剂量组中,甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)的水平显著降低(在AS-Ⅳ低剂量组中降低不显著)。②在AS-Ⅳ中、高剂量组中,TLR4、MYD88和TRAF6mRNA的表达水平明显下降(在AS-Ⅳ低剂量组中降低不显著)。③在AS-Ⅳ高、中剂量组中,TLR4、MyD88、TRAF6蛋白的表达水平显著下降(在AS-Ⅳ低剂量组中降低不显著)。④TLR4抑制剂TAK-242、MyD88抑制剂ST2825和TRAF6抑制剂C25-140能够抑制AS-Ⅳ的作用。结论AS-Ⅳ在HepG2高脂细胞中有降低血脂累积作用,可能通过减轻脂肪代谢障碍实现,其机理与Toll-like信号路径有关。Objective To discuss the effect of astragalosideⅣ(ASⅣ)on lipid metabolism in HepG2 cell model and the role of Toll-like signaling pathway in it.Methods HepG2 cells were used to construct hyperlipidemia model and randomly divided into six groups:low-,medium-and high-dose(0.05,0.1,0.2 mmol/L)AS-Ⅳgroups,control group,inhibitor group and AS-Ⅳ+inhibitor group.The expressions of Toll like receptor 4(TLR4),myeloid differentiation factor 88(MyD88),tumor necrosis factor receptor-associated factor 6,tumor necrosis factor receptor associated factor 6(TRAF6)mRNA and protein were detected by real-time quantitative polymerase chain reaction(PCR)and Western blot(WB)assay.Results①In high-dose AS-Ⅳgroup,the levels of triglycerides(TG),total cholesterol(TC)and low-density lipoprotein(LDL)were significantly reduced at high doses(not significantly reduced in the low-dose AS-Ⅳgroup).②In the medium-and high-dose AS-Ⅳgroups,the expression levels of TLR4,MYD88 and TRAF6 mRNA were significantly decreased(not significantly in lowdose group).③TLR4,MyD88,TRAF6 protein expression was significantly decreased in the high-and mediumdose AS-Ⅳgroups(not significantly in low-dose AS-Ⅳgroup).④TLR4 inhibitor TAK-242,MyD88 inhibitor ST2825 and TRAF6 inhibitor C25-140 were able to inhibit the action of AS-Ⅳ.Conclusion AS-Ⅳcan reduce the accumulation of blood lipids in HepG2 cells,which may be achieved by reducing the disorder of fat metabolism,and its mechanism is related to the Toll like signaling pathway.

关 键 词：黄芪甲苷 HepG2细胞 Toll-like通路 脂肪代谢 

分 类 号：R285[医药卫生—中药学]