羟基肉桂酸对HepG2和C2C12细胞糖脂代谢的调节作用

目的 研究羟基肉桂酸对HepG2细胞脂质堆积和葡萄糖消耗及C2C12细胞葡萄糖摄取的调节作用及其机制.方法 利用油酸诱导HepG2细胞建立脂质堆积模型,通过油红O染色法观察不同浓度羟基肉桂酸对脂质堆积的作用,并检测细胞内总胆固醇(TC)和甘油三酯(TG)含量;同时,采用MTT法检测羟基肉桂酸对细胞活力的影响;通过葡萄糖消耗实验和葡萄糖摄取实验检测羟基肉桂酸对细胞葡萄糖利用的影响;采用实时荧光定量PCR技术分析糖脂代谢关键基因的表达.结果 羟基肉桂酸能够显著抑制油酸诱导的HepG2细胞脂质堆积,同时降低细胞中TC和TG含量;羟基肉桂酸还能够显著增强细胞对葡萄糖的消耗,促进葡萄糖的摄取,显著降低固醇调节元件结合蛋白-1a、-1c、-2和脂肪酸合酶,乙酰辅酶A羧化酶和3-羟基-3-甲基戊二酸单酰辅酶A还原酶的mRNA表达水平,同时升高过氧化物酶体增殖物激活受体α(PPARα)的表达.结论羟基肉桂酸具有调节细胞糖脂代谢的作用,能够改善HepG2细胞中的脂质堆积,并且显著提高葡萄糖的利用率.其作用机制可能与激活PPAR等关键基因的表达有关.

Modulation of lipogenesis and glucose metabolism in HepG2 cells and C2C12 myotubes by hydroxycinnamic acid

Objective To investigate the effects and potential mechanism of hydroxycinnamic acid(HYD)on lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes. Methods The function of HYD on oleic acid(OA)elicited lipid ac-cumulation was measured by oil red O staining. Intracellular quantification of total cholesterol(TC)and triglycerides(TG)in HepG2 cells,and cell viability were observed by MTT assay. Additionally,glucose metabolic action of HYD was tested by glucose consump-tion in HepG2 cells and glucose uptake in C2C12 myotubes. The expression of glucose and lipid metabolism-related genes were detect-ed by real-time quantitative PCR(RT-PCR). Results Treatment with HYD significantly inhibited lipid accumulation in HepG2 cells in a dose-dependent manner without influence on cell viability. Meanwhile,HYD had the capability to increase glucose consumption in HepG2 cells and glucose uptake in C2C12 myotubes. Furthermore,RT-PCR revealed that the beneficial effect of HYD was associat-ed with the down-regulation of sterol regulatory element-binding proteins-1a,-1c,-2(SREBP-1a,SREBP-1c,and SREBP-2),fatty acid synthase(FAS),acetyl-CoA carboxylase(ACC),and hydroxyl methyglutaryl CoA reductase(HMGR),and up-regulation of per-oxisome proliferator-activated receptorα(PPARα). Conclusion HYD is an effective regulator of lipogenesis and glucose consump-tion. Up-regulation of PPAR may partially,if not wholly,participate in its beneficial effect.