【摘要】 目的：探讨中药复方糖肾方（TSF）调控非酒精性脂肪性肝病（NAFLD）细胞模型自噬改善脂质沉积的潜在机制。方法：棕榈酸（PA）诱导肝脏细胞HepG2发生脂质沉积，构建NAFLD细胞模型。使用BODIPY染色观察细胞脂质沉积的程度，免疫印迹法（Western blot）检测自噬标记物LC3B-Ⅰ/Ⅱ、自噬底物p62、沉默信息调节因子（SIRT1）、腺苷酸激活蛋白激酶（AMPK）以及自噬上游关键分子mTOR等信号通路蛋白的表达水平。结果：BODIPY染色结果显示，0.3mM PA可成功诱导NAFLD模型；与模型组相比，糖肾方显著降低肝细胞内脂质沉积，Western blot结果显示糖肾方显著上调自噬蛋白LC3BⅡ、SIRT1、p-AMPK的表达水平（P<0.05,P<0.01），显著降低p-mTOR和p62蛋白的表达水平（P<0.05,P<0.01）。结论：糖肾方可有效防治PA诱导的NAFLD细胞模型脂质沉积，其作用机制可能与促进细胞自噬和调控SIRT1/AMPK信号通路有关。更多还原

【Abstract】 Objective:To investigate the effect of Tangshen Formula(TSF)on autophagy in a HepG2 cell model of nonalcoholic fatty liver disease(NAFLD)and its possible mechanism for alleviating lipid deposition.Methods:Palmitic acid(PA)induced lipid deposition in HepG2 cells to construct an in vitro model of NAFLD.The extent of hepatocyte lipid deposition was observed using BODIPY,and Western blot was used to detect autophagy marker LC3B-Ⅰ/Ⅱ,autophagy substrate p62,silent information regulator 1(SIRT1),adenosine 5’-monophosphate(AMP)-activated protein kinase(AMPK),and mTOR,a key molecule upstream of autophagy.Results:The results of BODIPY staining showed that 0.3mM PA successfully induced NAFLD model,Western blot results showed that TSF particles significantly upregulated the expression levels of autophagy proteins LC3BⅡ,SIRT1 and p-AMPK(P<0.05,P<0.01)and significantly decreased the expression levels of p-mTOR and p62 proteins(P<0.05,P<0.01).Conclusion:Tangshen Formula could effectively combat lipid deposition in PA-induced cellular model of NAFLD,and its mechanism of action may be related to the promotion of autophagy and regulation of SIRT1/AMPK signaling pathway.更多还原