黄蜀葵花总黄酮介导AKT1信号通路拮抗HepG-2细胞脂质沉积研究  

Study on Total Flavonoids from Abelmoschus manihot L.Medic.Mediated AKT1 Signaling Pathway to Antagonize Against Lipid Deposition in HepG-2 Cells

作　　者：杨渊 鲍家成 戴宗英 YANG Yuan;BAO Jiacheng;DAI Zongying(Guangxi Key Laboratory of Environmental Exposure Omics and Life Cycle Health/School of Public Health,Guilin Medical College,Guilin Guangxi 541199,China)

机构地区：[1]广西全生命周期健康与保健研究重点实验室/桂林医学院公共卫生学院,广西桂林541199

出　　处：《中医药导报》2024年第6期29-33,共5页Guiding Journal of Traditional Chinese Medicine and Pharmacy

基　　金：广西科技计划项目(桂科AD21220070)。

摘　　要：目的:探讨黄蜀葵花总黄酮(TFA)对棕榈酸(PA)诱导HepG-2细胞脂质沉积模型的干预效应及机制。方法:体外培养人肝源HepG-2细胞,应用PA处理以构建细胞脂质沉积模型,然后从黄蜀葵花中提取TFA,以TFA或蛋白激酶B(AKT)抑制剂作为干预剂,对PA诱导的细胞脂质沉积模型进行预处理,应用油红O染色、酶联免疫吸附实验和免疫印迹实验(Western blotting)检测细胞脂质代谢、AKT1和脂联素(APN)信号通路蛋白表达水平。结果:与PA模型组比较,TFA或AKT抑制剂干预后,细胞脂质沉积程度(%)、游离脂肪酸(FFAs)和甘油三酯(TG)水平降低,而APN水平升高(P<0.05)。Western blotting实验显示PA模型组AKT1和固醇调节元件结合蛋白1(SREBP-1)表达水平上调而APN和糖原合成酶激酶3β(GSK3β)水平下调(P<0.05)。与PA模型组比较,TFA或AKT抑制剂干预显示AKT1下调而APN水平上调,其下游信号GSK3β表达上调而SREBP-1表达下调(P<0.05)。结论:TFA拮抗PA诱导的HepG-2细胞脂质沉积可能与其介导AKT1抑制及APN信号通路激活有关。Objective:To investigate the intervention effect and mechanism total flavones of Abelmoschus manihot L.Medic.(TFA)on lipid deposition model in HepG-2 cells induced by palmitic acid(PA).Methods:The cultivated human liver derived HepG-2 cells in vitro were treated by PA to construct a cellular lipid deposition model,and then TFA was extracted from Abelmoschus manihot L.Medic.And TFA or protein kinase B(AKT)inhibitors was used as pretreatment intervention agents,performing intervention against PA induced cellular lipid deposition model.Oil red O staining,enzyme-linked immunosorbent assay and Western blotting experiments were used to determine the expression levels of cellular lipid metabolism,AKT1 and adiponectin(APN)signaling pathway proteins.Results:Compared to PA model group,intervention with TFA or AKT inhibitor showed a significant decrease in the levels of cellular lipid deposition(%),free fatty acids(FFAs)and triglycerides(TG),while APN levels increased in HepG-2 cells(P<0.05).Western blotting experiments showed that the AKT1 and sterol regulatory element binding protein 1(SREBP-1)increased in PA model group,while levels of APN and glycogen synthase kinase 3β(GSK3β)decreased(P<0.05).Compared with PA model group,the intervention with TFA or AKT inhibitor showed the down-regulation of AKT1 while the up-regulation of APN,and its downstream signals SREBP-1 showed decreased expressions while GSK3βup-regulated(P<0.05).Conclusion:TFA may mediate the AKT1 inhibition and the activation of APN signaling pathway,to antagonize against PA-induced lipid deposition in HepG-2 cells.

关 键 词：黄蜀葵花总黄酮 AKT1 APN 脂质沉积 拮抗效应 HEPG-2细胞 

分 类 号：R285.5[医药卫生—中药学]