姜黄素对酒精诱导的HepG2细胞氧化损伤的保护作用  

Curcumin protects against alcohol-induced oxidative stress in human HepG2 cells

作　　者：孟凡东[1] 隋承光[1] 蒋涛[1] 王扬[1] 

机构地区：[1]中国医科大学附属第一医院肿瘤研究所二室,沈阳110001

出　　处：《解剖科学进展》2016年第2期165-168,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81202955)

摘　　要：目的探讨姜黄素在酒精诱导的Hep G2细胞氧化损伤中的保护作用,揭示姜黄素抗酒精性肝损伤的作用机制。方法不同浓度的姜黄素处理Hep G2细胞24 h后,加入酒精诱导细胞损伤。采用MTT检测姜黄素对损伤细胞活力的影响,试剂盒检测细胞中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量以及活性氧(ROS)水平,采用Real-time PCR检测SOD1、SOD2和CAT m RNA的表达。结果 300 mmol/L酒精可致近50%的细胞死亡,4μmol/L的姜黄素对酒精引起的细胞毒性作用保护效果最为显著,可明显改变细胞内SOD活性、MDA含量及ROS水平。与酒精组比较,4μmol/L的姜黄素可显著上调细胞内SOD1、SOD2和CAT m RNA的表达水平。结论姜黄素通过调节细胞的抗氧化能力削弱酒精对肝癌Hep G2细胞的损伤作用。Objective To assess the effect of curcumin as a antioxidant on alcohol-induced oxidative stress in HepG2 cells and to explore the possible mechanisms involved.Methods HepG2 cells were pretreated with curcumin for 24 h before treatment with alcohol to induce oxidative stress.MTT assay was performed to detect the viability of curcumin and alcohol treated HepG2 cells.Kits were used to detect the activity of superoxide dismutase（SOD）and the content of malondialdehyde（MAD）and the level of total intracellular reactive oxygen species（ROS）.Finally,Real-time PCR was performed to detect the mRNA expressions of SOD1,SOD2 and CAT.Results Treatment with 300 mmol/L alcohol without curcumin pretreatment resulted in the death of around 50% of cells,Curcumin at concentration 4 μmol/L had a significantly antagonistic effect against cytotoxicity of alcohol to HepG2 cells through the regulation of SOD activity and MDA content and ROS level,and increased the expression levels of SOD1,SOD2 and CAT mRNA in HepG2 cells.Conclusion Curcumin as an antioxidant protects against alcohol-induced oxidative stress by regulating the anti-oxidant capacity of HepG2 cells.

关 键 词：姜黄素 人HepG2细胞 酒精损伤 

分 类 号：R575.2[医药卫生—消化系统]