水飞蓟宾通过调控AMPK活性抑制自由脂肪酸诱导的肝细胞炎症因子分泌  

Silybin inhibits inflammatory cytokine secretion of hepatocytes induced by free fatty acid through regulating AMPK activity

作　　者：罗颂[1] 张羽[1] 何彦瑶 刘敏卓 LUO Song;ZHANG Yu;HE Yanyao;LIU Minzhuo(Department of Pharmacy,Hu′nan Children′s Hospital,Changsha 410007,China;Chemistry and Chemical Engineering,Central South University,Changsha 410083,China)

机构地区：[1]湖南省儿童医院药学部,长沙410007 [2]中南大学化学化工学院,长沙410083

出　　处：《西北药学杂志》2019年第1期72-75,共4页Northwest Pharmaceutical Journal

摘　　要：目的研究水飞蓟宾对自由脂肪酸(FFA)诱导肝细胞炎症因子分泌的抑制作用,并探讨其是否通过调节腺苷单磷酸活化蛋白激酶(AMPK)信号通路实现。方法将HepG2细胞分为对照组、模型组和水飞蓟宾组。水飞蓟宾组(80和160μmol·L-1)预孵育HepG2细胞4h后,用500μmol·L-1的FFA处理HepG2细胞24h。Real-time PCR和Elisa法测定炎症因子IL-1β和TNF-α的mRNA及蛋白表达,油红O染色检测脂质生成情况,Western Blot测定AMPK和p-AMPK的蛋白相对表达量。用AMPK抑制剂或水飞蓟宾孵育细胞后用FFA处理,Elisa法测定炎症因子的生成情况。结果水飞蓟宾组可降低FFA诱导炎症因子生成增加,降低肝细胞中脂质含量的积累。Western Blot测定结果发现,水飞蓟宾可增加AMPK的磷酸化,AMPK抑制剂可逆转水飞蓟宾对炎症因子生成的抑制作用。结论水飞蓟宾组可通过AMPK信号通路抑制FFA诱导肝细胞炎症因子的表达。Objective To investigate the inhibitory effects of silybin on the inflammatory factor secretion of HepG2 cells induced by free fatty acid(FFA)and to explore whether the underlying mechanism was associated with regulating adenosine monophosphate activated protein kinase(AMPK)signaling pathway.Methods HepG2 cells were divided into 3 groups:control group,model group and silybin group.After pre-incubated with silybin(80 and 160μmol·L^-1),HepG2 cells were treated with FFA(500μmol·L^-1)for 24 h.Real-time PCR and Elisa method were used to detect the level of mRNA and protein expression of IL-1βand TNF-α,respectively.The level of lipid accumulation was measured by oil-red O staining.The expression of AMPK and p-AMPK was detected by Western Blot.After incubation with silybin in the absence or presence of AMPK inhibitor,the HepG2 cells treated with FFA and the inflammatory factor levels were determined by Elisa method.Results Silybin can reduce the increased inflammatory cytokines production and reduce the accumulation of lipid content in HepG2 cells induced by FFA.Western Blot results showed that silybin increased the phosphorylation of AMPK in HepG2 cells treated with FFA,and the AMPK inhibitors reversed the inhibitory effect of silybin on the FFA-induced inflammatory factors production.Conclusion Silybin decreased the HepG2 cells inflammatory cytokines expression induced by FFA via inhibiting AMPK activity.

关 键 词：水飞蓟宾 非酒精性脂肪肝 炎症因子 腺苷单磷酸活化蛋白激酶 

分 类 号：R965[医药卫生—药理学]