中药组分HJJB方对油酸钠诱导的HepG2细胞脂质沉积的干预作用及机制

Intervention and mechanism of HJJB Formula on lipid accumulation in HepG2 cells induced by sodium oleate

目的:观察HJJB方[由红景天苷(H)、绞股蓝总苷(J)、姜黄素(J)、白术多糖(B)特定配比组成]对油酸钠诱导的HepG2细胞脂质沉积的干预作用,并探讨HJJB方抑制细胞脂质沉积的作用机制。方法:运用油酸钠诱导的HepG2细胞脂肪变性模型,在确定药物无毒性剂量范围的前提下,设正常组、模型组、HJJB方组和罗格列酮组,观察细胞上清液中胰岛素、葡萄糖和肿瘤坏死因子α(TNF-α)含量;细胞内甘油三酯(TG)含量及油红O染色;细胞内脂肪酸合成酶(FAS)、乙酰辅酶A羧化酶(ACCase)、丙二酰辅酶A(Malonyl-Co A)蛋白含量。结果:模型组细胞内TG、FAS、ACCase、Malonyl-CoA含量和细胞上清液中胰岛素、葡萄糖、TNF-α水平较正常组显著升高(P<0.01),HJJB方组和罗格列酮组的上述指标均显著降低(P<0.01),HJJB方组的细胞内TG、FAS、ACCase、Malonyl-Co A含量和细胞上清液中胰岛素、TNF-α水平显著低于罗格列酮组(P<0.01)。结论:HJJB方对油酸钠诱导的Hep G2细胞脂质沉积具有明显的抑制作用,其机制与抑制脂质合成和增强胰岛素敏感性有关。

Objective:To observe the intervention effect of HJJB Formula[it was formed by salidroside(H),gypenoside(J),curcumin(J),atractylodes macrocephala ploysacharide(B)according to specific proportion]on sodium oleate induced lipid deposition in HepG2 cells,and to discuss the mechanism of HJJB Formula inhibiting cell fat deposition.Methods:Using HepG2 cell steatosis model induced by sodium oleate,normal group,model group,HJJB Formula group and rosiglitazone group were set up on the premise of determining the range of non-toxic doses of drugs.The observing items including:contents of insulin,glucose and tumor necrosis factor-alpha(TNF-α)in cell supernatants;intracellular triglyceride(TG)content and oil red O staining;intracellular fatty acid synthase(FAS),acetyl coenzyme A carboxylase(ACCase)and malonyl coenzyme A(Malonyl-CoA)protein content.Results:The intracellular TG,FAS,ACCase,Malonyl-CoA content and the cell supernatant insulin,glucose and TNF-a levels of model group were significantly higher than that of normal group(P<0.01).The above indexes of HJJB Formula group and rosiglitazone group were significantly lower(P<0.01).The intracellular TG,FAS,ACCase,Malonyl-CoA contents and the cell supernatant insulin,TNF-αlevels of HJJB Formula group were significantly lower than that of rosiglitazone group(P<0.01).Conclusion:HJJB Formula can inhibit the lipid deposition of HepG2 cells induced by sodium oleate,and its mechanism is related to inhibiting lipid synthesis and enhancing insulin sensitivity.