摘要
研究甲状腺激素(T3)对人肝癌细胞(HepG2)氧化损伤的保护作用。体外建立HepG2细胞H2O2氧化损伤模型,添加不同浓度T3进行保护,测定T3对细胞ROS、存活率、抗氧化酶及相关基因的影响。10-9、10-7、10-5mol/L的T3预处理24 h可分别有效降低50、100、200μmol/L H2O2处理细胞的ROS水平,提高细胞存活率(p<0.05)。但10-5mol/L的T3反而会增加50μmol/L H2O2处理细胞的ROS水平,降低存活率(p<0.05)。适量T3可显著降低H2O2氧化损伤的HepG2细胞MDA含量(p<0.05),显著提高T-AOC、GSH-Px以及SOD活性(p<0.05)。但过量T3会增加细胞MDA水平,降低酶活。基因表达也有类似趋势,T3预处理使损伤细胞内PI3K、Nrf2的表达显著提高(p<0.05),且与T3作用剂量相关。可见T3对H2O2氧化损伤的HepG2细胞的氧化还原状态具有明显的改善作用,其抗氧化保护功能与提高抗氧化酶的活性及细胞内抗氧化相关基因的表达有关,且T3作用效果与其剂量及细胞损伤水平相关。
To investigate the protect effects of thyroid hormone （T3） on HepG2 with oxidative damage.Establishing an oxidative stress model of HepG2 cells cultured in vitro,adding different concentrations of T3 for protection,determining the differentiation of cellular ROS,survival,antioxidant enzymes and related genes.Pretreatment of 10-9,10-7,10-5 mol/L T3 for 24 h,the level of ROS significantly reduced and the survival rate of cells was significantly increased（p＜0.05）in cells of 50,100,200 μmol/L H2O2 processing respectively.While,10-5 mol/L T3 increased the level of ROS.The amount of T3 can significantly reduce MDA content （p＜0.05）,increase T-AOC,GSH-Px and SOD activity of cells of H2O2 oxidative damage（p＜0.05）.But excess T3 increased MDA content and decreased the antioxidant activity.The results of gene expression showed that T3 pretreatment significantly increased PI3K,Nrf2 in the damaged cells（p＜0.05）.T3 can improve the redox state of HepG2 cells of H2O2 oxidative damage because of the effect on antioxidant enzyme activities and the expression of anti-oxidation genes and the effect is related to the dose and cell damage levels.
出处
《食品与生物技术学报》
CAS
CSCD
北大核心
2014年第9期935-940,共6页
Journal of Food Science and Biotechnology
基金
国家"十二五"科技支撑计划项目(2012BAD33B05)
江苏高校优势学科建设工程资助项目
作者简介
通信作者施用晖（1955-）,女,上海人,农学博士,教授,博士研究生导师,主要从事营养代谢调控研究.E-mail：yhshi@jiangnan.edu.cn
