降脂理肝汤对体外诱导的非酒精性脂肪肝细胞模型SREBP-1c通路的影响

Effect of Jiangzhi Ligan Decoction on SREBP-1c Pathway in the Nonalcoholic Fatty Liver Disease (NAFLD) Cell Model Induced in Vitro

目的:观察降脂理肝汤对油酸诱导的HepG2细胞中固醇调节元件结合蛋白1c(sterol regulatory element binding protein-1c,SREBP-1c)通路相关蛋白表达的影响,探讨降脂理肝汤治疗非酒精性脂肪肝的可能机制。方法:采用油酸诱导HepG2细胞建立非酒精性脂肪肝细胞模型,降脂理肝汤4 mg/ml和阿托伐他汀0.005 mg/ml干预后,利用油红O染色定性定量检测细胞内脂质蓄积情况;试剂盒检测细胞内TG、TC和FFA水平;Western bolt观察和分析细胞p-SREBP-1c、SREBP-1c、FAS、ACC1和SCD1蛋白表达的变化。结果:油酸诱导的HepG2细胞脂质蓄积明显;细胞内TG、TC和FFA含量明显升高,细胞p-SREBP-1c蛋白表达水平显著下调,SREBP-1c、FAS、ACC1和SCD1蛋白表达水平显著上调。降脂理肝汤和阿托伐他汀干预显著降低油酸诱导的HepG2细胞TG、TC和FFA含量。细胞SREBP-1c、FAS、ACC1和SCD1蛋白表达显著下调;此外,降脂理肝汤干预显著减少油酸诱导的HepG2细胞脂质蓄积,显著上调细胞p-SREBP-1c蛋白表达水平。结论:降脂理肝汤可能通过抑制SREBP-1c通路干预NAFLD。

Objective:To study the effect of Jiangzhi Ligan Decoction on SREBP-1 c pathway in cell model with nonalcoholic fatty liver disease(NAFLD),thus to explore the possible mechanism of Jiangzhi Ligan Decoction on NAFLD.Methods:HepG2 cells model with NAFLD was established by oleic acid(OA).After the intervention of Jiangzhi Ligan Decoction(4 mg/ml)or Atorvastatin(0.005 mg/ml),the lipid accumulation was detected qualitatively and quantitatively by oil red O staining,the levels of TG,TC and FFA were measured by the detection kits,the protein expressions levels of p-SREBP-1 c,SREBP-1 c,FAS,ACC1 and SCD1 were determined by Western bolt.Results:Lipid accumulation,the levels of TG,TC and FFA,the protein expression levels of SREBP-1 c,FAS,ACC1 and SCD1 were significantly increased in OA-induced HepG2 cells,the protein expression level of p-SREBP-1 c was significantly decreased in OA-induced HepG2 cells.The levels of TG,TC and FFA,the protein expression levels of SREBP-1 c,FAS,ACC1 and SCD1 were significantly decreased in OA-induced HepG2 cells after the intervention of Jiangzhi Ligan Decoction and Atorvastatin.The intervention of Jiangzhi Ligan Decoction significantly reduced lipid accumulation and increased the protein expression level of p-SREBP-1 c in OA-induced HepG2 cells.Conclusion:Jiangzhi Ligan Decoction can improve NAFLD by inhibiting SREBP-1 c pathway.