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目的 探讨花色苷单体矢车菊素-3-葡萄糖苷(Cy-3-g)对HepG2细胞脂肪含量的影响以及可能机制.方法 HepG2细胞分别用1、10、100 μmol/Lcy-3-g处理1h,设置对照,检测腺苷-磷酸激活蛋白激酶(AMPK)及其磷酸化水平、肉碱脂酰转移酶-Ⅰ(CPT-Ⅰ)、乙酰辅酶A羧化酶(ACC)磷酸化水平、AMPK活性、甘油三酯含量以及脂肪酸氧化水平.结果 与对照组相比,显著上调CPT-Ⅰ蛋白的表达水平,显著增强AMPK的活性,显著促进AMPK蛋白磷酸化,但对AMPK蛋白表达水平无影响,显著减少HepG2细胞内的甘油三酯含量,10、100 μmol/L Cy-3-g能显著促进ACC的磷酸化,100 μmol/L Cy-3-g能显著促进HepG2细胞脂肪酸氧化.结论 花色苷Cy-3-g可以减少HepG2细胞脂肪积聚;其机制可能与调节HepG2细胞AMPK-ACC-CPT-Ⅰ信号通路,促进脂肪酸氧化有关.“,”Objective To study the effects of anthocyanins on hepatic lipid accumulation and to explore the possible mechanisms. Method HepG2 cells were treated with 1, 10 and 100 umol/L cyanidin-3-0-β-glucoside (Cy-3-g) for lh, carnitine palmitoyl transferase- I (CPT-I) protein level and acetyl CoA carboxylase (ACC) phosphorylation, triglyceride, fatty acid oxidation, the activity of AMPK, AMPK and p-AMPK protein levels were evaluated. Results Compared with the control, the treatment of HepG2 with 1, 10, 100 umol/L Cy-3-g resulted in significant decrease of intracellular triglyceride, and significant increase of CPT- I protein, and AMPK activity and phosphorylation. However, there were no differences in AMPK protein level among all groups. The treatment of 100 umol/L Cy-3-g promoted the fatty acid oxidation in HepG2. The treatment of 10,100 nmol/L Cy-3-g significantly increased ACC phosphorylation. Conclusion Anthocyanin Cy-3-g could attenuate hepatic lipid accumulation in HepG2. The mechanism may result from the regulation of the AMPK-ACC- CPT-I signal pathway and promotion of fatty acid oxidation.