摘要
研究圣草酚体外清除自由基的活性；采用2,2-偶氮二（2-甲基丙基咪）二盐酸盐（AAPH）诱导牛血清白蛋白（BSA）、大鼠肝组织及质粒DNA构建过氧化反应模型，以蛋白羰基化、丙二醛（MDA）生成量和DNA断裂为指标，研究圣草酚对自由基损伤蛋白质、脂质、DNA 3种生物大分子的作用；通过MTT法检测圣草酚对肝癌细胞HepG2的毒性。结果表明：25～200μmol/L的圣草酚具有较强的DPPH自由基清除作用，IC50值为95.7μmol/L，但清除羟自由基能力较弱。圣草酚呈浓度依赖性抑制脂质、蛋白质、DNA的氧化损伤。400μmol/L的圣草酚作用48h能显著地降低肝癌细胞HepG2细胞活力。结论：圣草酚能有效地清除DPPH自由基，抑制自由基损伤生物大分子及肝癌细胞HepG2的活力。
The in vitro free radical-scavenging activity of eriodictyol was evaluated against DPPH and hydroxyl free radicals. The protective effect of eriodictyol on free radical-induced damage to protein, lipid and DNA were evaluated based on oxidation models of BSA, rat liver tissue and plasmid DNA induced by AAPH and its cytotoxicity on HepG2 cells was assessed by MTT assay. The results showed that eriodictyol in the concentration range of 25 to 200 μmol/L had strong scavenging activity against DPPH free radical with a median inhibitory concentration （IC50） of 95.7 μmol/L. However, the scavenging activity on hydroxyl free radical was weaker. The inhibitory effect of eriodictyol on oxidative damage to protein, lipid and DNA induced by free radicals was in a dose-dependent manner. Similarly, eriodictyol could significantly reduce the viability of HepG2 cells in a dose-dependent manner. Therefore, eriodictyol has the capability to scavenge DPPH free radicals and inhibit macromolecular damage induced by free radicals. It also can significantly reduce the viability of HepG2 cells.
出处
《食品科学》
EI
CAS
CSCD
北大核心
2013年第17期126-130,共5页
Food Science
关键词
圣草酚
自由基
蛋白损伤
脂质过氧化
DNA断裂
细胞毒性
eriodictyol
free radical
protein damage
lipid peroxidation
DNA strand breakage
cytotoxicity
