CAJ | 학술논문

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P4504A11（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HepG2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。
탐토곡피소-3-O-β-D-포도당철산감（ quercetin-3-O-β-D-glucuronide，Q3GA）대유리지방산유도적인원간암세포HepG2세포지질축적적감유삼지조절화양화응격적작용급기가능적상관궤제。채용유홍염색검측Q3GA대유리지방산유도적HepG2세포중지적함량적영향，병동시검측기대감유삼지화담고순적작용。 DCFH-DA법검측Q3GA대HepG2세포지질축적인기적활성양（ ROS）적변화；류대파비타산법화황표령양화매법분별측정병이철（ MDA）적함량화초양화물기화매（ SOD）적활성。 RT-PCR분석지방산양화상관적기인과양화물매체증식물수체（ PPARα）、육독감종려선전이매（CPT1A）、중련선기보매A탈경매（MCAD）、세포색소P4504A11（CYP4A11）、을선보매A양화매（ACO）적표체정황。실험결과현시，Q3GA가제량의뢰성강저FFA유도적HepG2세포지질축적화감유삼지적함량，단미강저담고순적함량。동시가개선지방산양화인기ROS，MDA적승고이급SOD적강저。령외，Q3GA재일정농도하가상조지방산β양화상관기인PPARα、CPT1A、MCAD적표체，이대CYP4A11화ACO적표체몰유촉진작용。종상소술，Q3GA가저항지방산양화인발간세포적양화응격손상，보호HepG2세포，강저유리지방산유도HepG2세포지질축적화감유삼지적함량，기조절궤제가능여기대HepG2세포중유리지방산양화유관。
The effects of quercetin-3-O-β-D-glucuronide (Q3GA)on the triglyceride metabolism and oxidative stress in steatotic HepG2 cells and the underlying mechanism were investigated in this study.Significant fat accu-mulation was documented by Oil Red O staining;intracellular triglyceride levels were detected by triglyceride(TG)enzymatic assay.DCFH-DA staining assay was performed to observe reactive oxygen species (ROS)pro-duction of HepG2 cells.The level of malondialdehyde(MDA)and superoxide dismutase(SOD)were assayed by thibabituric acid method and xanthine oxidase method.Changes in the mRNA expression of peroxisome prolifera-tor-activated receptorα(PPARα);carnitine palmitoyltransferase 1 A(CPT1 A);medium chain acyl-CoA dehydro-genase (MCAD);cytochrome P450 4A11(CYP4A11)and acyl-CoA oxidase(ACO);which are related with fatty acid oxidation were assessed by RT-PCR.Our results showed that Q3GA obviously reduced fat deposition and TG content.At the same time;Q3 GA decreased MDA content and significantly increased the SOD activity with reduced ROS production.Moreover;the PPARα;CPT1A;MCAD expression-related fatty acid βoxidation was upregulated with the treament of Q3GA;while without any change of the expression of CYP4A11;ACO.In conclu-sion;Q3GA prevents FFA-induced HepG2 cell steatosis;and enhances mitochondrial fatty acidβoxidation;which may partly be related to its anti-oxidation ability.