姜黄素对HepG2细胞脂质沉积的改善作用及机制研究

Study on the improvement and mechanism of curcumin on lipid deposition in HepG2 cells

目的:探讨姜黄素对油酸诱导的HepG2细胞脂质沉积的影响及其作用机制。方法:将HepG2细胞分为对照组、模型组及姜黄素低、高剂量组。除对照组外,其他3组给予0.3 mmol/L油酸干预24 h,诱导细胞脂质沉积模型。造模后,姜黄素干预组分别予以50、100μmol/L姜黄素干预9 h。油红O染色观察各组细胞内脂质沉积情况,试剂盒检测细胞内三酰甘油(TG)和总胆固醇(TC)含量,PCR检测各组细胞固醇调节元件结合蛋白1C(SREBP1C)、脂肪酸合成酶(FAS)、乙酰辅酶A羧化酶α(ACCα)的mRNA表达。结果:与对照组相比,模型组细胞内脂滴明显增多,TG、TC水平显著升高(P<0.05,P<0.01),SREBP1C及其下游基因FAS、ACCα的mRNA表达水平均显著升高(P<0.01)。与模型组相比,姜黄素干预组细胞内的红色脂滴明显减少,TG水平显著降低(P<0.01),SREBP1C、FAS、ACCα的mRNA表达水平均显著下调(P<0.05,P<0.01)。姜黄素低剂量(50μmol/L)对脂质沉积的改善作用更为显著。结论:姜黄素或通过下调SREBP1C、FAS、ACCα的表达,抑制脂质的合成,进而改善HepG2细胞的脂质沉积。

Objective: To investigate the effects of curcumin on oleic acid induced lipid deposition in HepG2 cells, as well as its mechanism. Methods: HepG2 cells were divided into the control group, model group, and curcumin low-and high-dose groups. Except the control group, the other groups were treated with 0.3 mmol/L oleic acid for 24 hours to induce cell lipid deposition model. After the model was established, curcumin intervention groups were treated with 50 and 100 μmol/L curcumin for 9 hours, respectively. Lipid deposition was observed by oil red O staining. The contents of triglyceride(TG) and total cholesterol(TC) were detected by the kits. The mRNA expressions of sterol-regulatory element binding protein 1 C(SREBP1 C), fatty acid synthetase(FAS) and acetyl CoA carboxylase α(ACCα) were detected by PCR. Results: Compared with the control group, the lipid droplets in the model group were significantly increased, the levels of TG and TC were significantly increased(P<0.05,P<0.01), and the mRNA expression levels of SREBP1 C and its downstream genes FAS and ACCα were significantly increased(P<0.01). Compared with the model group, the red lipid droplets in the curcumin intervention groups were significantly reduced, the TG level was significantly decreased(P<0.01), and the mRNA expression levels of SREBP1 C, FAS and ACCα were significantly decreased(P<0.05, P<0.01). The improvement on lipid deposition was more significantly in the curcumin low-dose(50 μmol/L) group. Conclusion: Curcumin may inhibit the lipid synthesis by down-regulating the expressions of SREBP1 C, FAS and ACCα, and thus improve the lipid deposition of HepG2 cells.