Jiao Hong-Li, Ye Ping, Zhao Bao-Lu
Laboratory of Visual Information Processing, Research Centers of Brain and Cognitive Science, Institute of Biophysics, The Chinese Academy of Sciences, Beijing, China.
Free Radic Biol Med. 2003 Nov 1;35(9):1121-8. doi: 10.1016/s0891-5849(03)00506-9.
The aim of this work was to investigate the protective effects of green tea polyphenols on the cytotoxic effects of hypolipidemic agent fenofibrate (FF), a peroxisome proliferator (PP), in human HepG2 cells. The results showed that high concentrations of FF induced human HepG2 cell death through a mechanism involving an increase of reactive oxygen species (ROS) and intracellular reduced glutathione (GSH) depletion. These effects were partially prevented by antioxidant green tea polyphenols. The elevated expression of PP-activated receptors alpha (PPARalpha) in HepG2 cells induced by FF was also decreased by treatment with green tea polyphenols. In conclusion, this result demonstrates that oxidative stress and PPARalpha are involved in FF cytotoxicity and green tea polyphenols have a protective effect against FF-induced cellular injury. It may be beneficial for the hyperlipidemic patients who were administered the hypolipidemic drug fenofibrate to drink tea or use green tea polyphenols synchronously during their treatment.
本研究旨在探讨绿茶多酚对降血脂药物非诺贝特(FF)——一种过氧化物酶体增殖剂(PP)——在人肝癌细胞HepG2中细胞毒性作用的保护效果。结果显示,高浓度的FF通过一种涉及活性氧(ROS)增加和细胞内还原型谷胱甘肽(GSH)耗竭的机制诱导人HepG2细胞死亡。抗氧化剂绿茶多酚可部分预防这些效应。FF诱导的HepG2细胞中过氧化物酶体增殖物激活受体α(PPARα)的表达升高也因绿茶多酚处理而降低。总之,该结果表明氧化应激和PPARα参与了FF的细胞毒性作用,且绿茶多酚对FF诱导的细胞损伤具有保护作用。对于接受降血脂药物非诺贝特治疗的高脂血症患者而言,在治疗期间同步饮茶或使用绿茶多酚可能有益。