原儿茶醛对叔丁基过氧化氢损伤HepG2细胞的保护作用  

Protection of protocatechuic aldehyde against HepG2 cells injury induced by tert-butyl hydroperoxide

作　　者：叶志华[1] 邢雅玲[1] 田琳琳[1] 周喆[1] 王升启[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所

出　　处：《军事医学科学院院刊》2007年第2期126-129,共4页Bulletin of the Academy of Military Medical Sciences

基　　金：国家自然科学基金重点项目(30530650);国家杰出青年基金项目(30625041)

摘　　要：目的:考察原儿茶醛(PCA)对氧化损伤HepG2细胞的保护作用及其作用机制。方法:200μmol/L叔丁基过氧化氢(t-BHP)损伤HepG2细胞,检测不同浓度原儿茶醛对细胞活力、超氧化物歧化酶活性、细胞内还原型谷胱甘肽及活性氧族的影响。结果:200μmol/L叔丁基过氧化氢可以显著性地损伤HepG2细胞,原儿茶醛给药能够显著提高损伤细胞的活力、提升超氧化物歧化酶的活性、降低细胞内活性氧族的含量、增加细胞内还原型谷胱甘肽的含量。结论:原儿茶醛对HepG2细胞有保护作用,其作用机制可能是通过提高抗氧化酶活性、加快活性氧的清除实现细胞保护作用。Objective： To investigate the protective effect of protocatechuic aldehyde（PCA） against HepG2 cells injury induced by tert-butyl hydroperoxide（t-BHP） and its mechanism. Methods：HepG2 cells were injured by 200 μmol/L t- BHP and different final concentrations of protocatechuic aldehyde （150 μmol/L,50μmol/L, 17 μmol/L） were added. Cell viability and superoxide dismutase（ SOD）, reactive oxygen species （ROS）, reduced glutathione （GSH） in the ceils were measured. Results： 200 μmol/L t-BHP caused HepG2 injury significantly, PCA could significantly improve cell viability, enhance SOD activity, reduce ROS and increase GSH in HepG2 cell. Conclusion： PCA （150 μmol/L）shows protective effect on HepG2 cells injured by t-BHP.

关 键 词：丹参 原儿茶醛 叔丁基氢过氧化物 癌 肝细胞 超氧化物歧化酶 HEPG2 

分 类 号：R285[医药卫生—中药学]