黄芩苷对高脂诱导HepG2细胞脂肪沉积及SIRT1相关因子表达的影响

目的 研究黄芩苷(Baicalin,BA)对游离脂肪酸(FFA)诱导HepG2细胞脂肪沉积的影响及机制研究.方法 选用0.75mmol/L的FFA体外诱导HepG2细胞24h,建立体外脂肪沉积模型.将细胞分为正常组、模型组、黄芩苷低、中、高剂量组.利用油红O染色及GPO-PAP酶法检测各组细胞内甘油三酯(TG)含量的变...

Effects of Baicalin on High Fat-Induced Lipid Accumulation and SIRT1 Related Factors Expression of HepG2 Cells in vitro

OBJECTIVE To study the effects and mechanism of baicalin on high fat-induced lipid accumulation in HepG2 cells.METHODS HepG2 cells were induced in vitro with 0.75 mmol/L free fatty acid for 24 h to establish an in vitro fat deposition model.The cells were then divided into the following groups;normal group,model group,50μmol/L baicalin group,100μmol/L baicalin group and 200μmol/L baicalin group.Oil Red O staining and GPO-PAP enzymatic method were used to detect the changes of TG content in each group of cells,and enzyme-linked immunosorbent assay(ELISA)was used to detect inflammatory factors in the supernatant of each group:TNF-α,IL-6.Western Blot was used to detect the following protein content:SIRT1,ChREBP,SREBP1c,FAS Protein.RESULTS Free fatty acid induced lipid accumulation in HepG2 cells increased,the concentration of TG in cells increased significantly;after the drug intervention,the intracellular lipid droplets in the three drug groups were reduced in comparison to the model group,therefore,showing drug-concentration-dependent results;the TG concentration showed a downward trend in the drug-groups,in which,the differences between the 100μmol/L and 200μmol/L drug group and the model group were statistically significant(P<0.05).Western blot detection showed that compared with the normal group,the expression of SIRT1 protein in the model group was significantly reduced,and the protein expressions of SREBP-1c and FAS increased significantly;the SIRT1 protein expressions of the cells in the 100μmol/L baicalin group and 200μmol/L baicalin group increased significantly,while SREBP-1c,ChREBP and FAS protein expression decreased significantly(P<0.05).CONCLUSION Baicalin can reduce the lipid accumulation of HepG2 cells induced by free fatty acids and reduce the TG content in the cells.The mechanism may be related to the SIRT1/SREBP-1c pathway.