槲皮素-3-O-β-D-葡萄糖醛酸苷对游离脂肪酸诱导HepG2细胞脂肪变性的作用

发布时间：2018-06-15 03:35

  本文选题：槲皮素--O-β-D-葡萄糖醛酸苷 + HepG细胞　； 参考：《中国药科大学学报》2015年05期

【摘要】：探讨槲皮素-3-O-β-D-葡萄糖醛酸苷(quercetin-3-O-β-D-glucuronide,Q3GA)对游离脂肪酸诱导的人源肝癌细胞HepG2细胞脂质蓄积的甘油三酯调节和氧化应激的作用及其可能的相关机制。采用油红染色检测Q3GA对游离脂肪酸诱导的HepG2细胞中脂滴含量的影响,并同时检测其对甘油三酯和胆固醇的作用。DCFH-DA法检测Q3GA对HepG2细胞脂质蓄积引起的活性氧(ROS)的变化;硫代巴比妥酸法和黄嘌呤氧化酶法分别测定丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活性。RT-PCR分析脂肪酸氧化相关的基因过氧化物酶体增殖物受体(PPARα)、肉毒碱棕榈酰转移酶(CPT1A)、中链酰基辅酶A脱氢酶(MCAD)、细胞色素P450 4A11(CYP4A11)、乙酰辅酶A氧化酶(ACO)的表达情况。实验结果显示,Q3GA可剂量依赖性降低FFA诱导的Hep G2细胞脂质蓄积和甘油三酯的含量,但未降低胆固醇的含量。同时可改善脂肪酸氧化引起ROS,MDA的升高以及SOD的降低。另外,Q3GA在一定浓度下可上调脂肪酸β氧化相关基因PPARα、CPT1A、MCAD的表达,而对CYP4A11和ACO的表达没有促进作用。综上所述,Q3GA可抵抗脂肪酸氧化引发肝细胞的氧化应激损伤,保护HepG2细胞,降低游离脂肪酸诱导HepG2细胞脂质蓄积和甘油三酯的含量,其调节机制可能与其对HepG2细胞中游离脂肪酸氧化有关。
[Abstract]:To investigate the effects of quercetin-3-O- 尾 -D-glucuronide-Q3GAon triglyceride on lipid accumulation and oxidative stress in HepG2 cells induced by free fatty acids. The effects of Q3GA on lipid droplets in HepG2 cells induced by free fatty acids were detected by oil red staining. The effects of Q3GA on lipids and cholesterol in HepG2 cells were also detected. DCFH-DA method was used to detect the changes of reactive oxygen species (Ros) induced by lipid accumulation in HepG2 cells. Determination of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) by thiobarbituric acid method and xanthine oxidase method. RT-PCR analysis of peroxisome proliferator receptor PPAR 伪, carnitine palmityl transfer The expression of CPT1AX, MCADN, CYP4A11, and ACOs were observed in the medium chain coenzyme A dehydrogenase (MCADN), cytochrome P450 4A11 (CYP4A11) and acetyl coenzyme A oxidase (ACO). The results showed that Q3GA decreased lipid accumulation and triglyceride content in FFA induced Hep G2 cells in a dose-dependent manner, but did not decrease cholesterol content. At the same time, it can improve the increase of MDA and the decrease of SOD caused by oxidation of fatty acid. In addition, Q3GA upregulated the expression of PPAR 伪 -CPT1A1MCAD at a certain concentration, but did not promote the expression of CYP4A11 and ACO. In conclusion, Q3GA can resist oxidative stress injury induced by fatty acid oxidation, protect HepG2 cells, and decrease lipid accumulation and triglyceride content in HepG2 cells induced by free fatty acids. The mechanism may be related to the oxidation of free fatty acids in HepG2 cells.
【作者单位】： 中国药科大学新药筛选中心;
【基金】：“十二五”国家科技支撑计划资助项目(No.2012BAI30B01)~~
【分类号】：R575.5
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本文编号：2020438