本文選題：槲皮素--O-β-D-葡萄糖醛酸苷 + HepG細(xì)胞　； 參考：《中國(guó)藥科大學(xué)學(xué)報(bào)》2015年05期

【摘要】：探討槲皮素-3-O-β-D-葡萄糖醛酸苷(quercetin-3-O-β-D-glucuronide,Q3GA)對(duì)游離脂肪酸誘導(dǎo)的人源肝癌細(xì)胞HepG2細(xì)胞脂質(zhì)蓄積的甘油三酯調(diào)節(jié)和氧化應(yīng)激的作用及其可能的相關(guān)機(jī)制。采用油紅染色檢測(cè)Q3GA對(duì)游離脂肪酸誘導(dǎo)的HepG2細(xì)胞中脂滴含量的影響,并同時(shí)檢測(cè)其對(duì)甘油三酯和膽固醇的作用。DCFH-DA法檢測(cè)Q3GA對(duì)HepG2細(xì)胞脂質(zhì)蓄積引起的活性氧(ROS)的變化;硫代巴比妥酸法和黃嘌呤氧化酶法分別測(cè)定丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活性。RT-PCR分析脂肪酸氧化相關(guān)的基因過(guò)氧化物酶體增殖物受體(PPARα)、肉毒堿棕櫚酰轉(zhuǎn)移酶(CPT1A)、中鏈酰基輔酶A脫氫酶(MCAD)、細(xì)胞色素P450 4A11(CYP4A11)、乙酰輔酶A氧化酶(ACO)的表達(dá)情況。實(shí)驗(yàn)結(jié)果顯示,Q3GA可劑量依賴性降低FFA誘導(dǎo)的Hep G2細(xì)胞脂質(zhì)蓄積和甘油三酯的含量,但未降低膽固醇的含量。同時(shí)可改善脂肪酸氧化引起ROS,MDA的升高以及SOD的降低。另外,Q3GA在一定濃度下可上調(diào)脂肪酸β氧化相關(guān)基因PPARα、CPT1A、MCAD的表達(dá),而對(duì)CYP4A11和ACO的表達(dá)沒(méi)有促進(jìn)作用。綜上所述,Q3GA可抵抗脂肪酸氧化引發(fā)肝細(xì)胞的氧化應(yīng)激損傷,保護(hù)HepG2細(xì)胞,降低游離脂肪酸誘導(dǎo)HepG2細(xì)胞脂質(zhì)蓄積和甘油三酯的含量,其調(diào)節(jié)機(jī)制可能與其對(duì)HepG2細(xì)胞中游離脂肪酸氧化有關(guān)。
[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 偽, 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 偽 -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.
【作者單位】： 中國(guó)藥科大學(xué)新藥篩選中心;
【基金】：“十二五”國(guó)家科技支撐計(jì)劃資助項(xiàng)目(No.2012BAI30B01)~~
【分類號(hào)】：R575.5
，

本文編號(hào)：2020438