文献类型：期刊文献

中文题名：构树总黄酮诱导HepG2细胞凋亡及其机理研究

英文题名：Study of the mechanism of the apoptosis of HepG2 induced by total flavonoids from Broussonetia papyrifera

作者：豆沉着[1];赵云涛[2];陈绍红[2];刘铀[2];刘艳芬[1]

机构：[1]广东海洋大学农学院,湛江524088;[2]广东海洋大学生物化学实验中心,湛江524088

年份：2016

卷号：32

期号：6

起止页码：109

中文期刊名：中药药理与临床

外文期刊名：Pharmacology and Clinics of Chinese Materia Medica

收录：北大核心2014、CSCD2015_2016、北大核心、CSCD

基金：广东省农业科技计划项目(0809035):构树综合加工利用技术研究

语种：中文

中文关键词：构树总黄酮;Hep;G2细胞;凋亡;基因表达;氧化应激

外文关键词：total flavonoids of Broussonetia papyrifera（构树总黄酮） ; HepG2 cells; apoptosis; gene expression; oxidative stress

中文摘要：目的:探讨构树总黄酮诱导HepG2细胞凋亡的机理。方法:采用流式细胞术观察构树总黄酮对HepG2细胞周期、细胞内活性氧(ROS)水平的影响,用qRT-PCR测定c-Myc,p53,bax,bcl-2和caspase-3基因mRNA表达水平的变化。结果:构树总黄酮剂量依赖性抑制HepG2细胞增殖。62.5μg/ml的构树总黄酮作用24 h,显著抑制HepG2细胞增殖,增加凋亡细胞比例,并将HepG2细胞阻滞于G1期;100μg/ml的构树总黄酮作用24 h,显著上调HepG2细胞p53、bax、caspase-3的mRNA水平,显著下调cMyc、bcl-2的mRNA水平;200μg/ml的构树总黄酮作用HepG2细胞6 h,显著增加细胞内ROS含量。结论:构树总黄酮能调节HepG2细胞c-Myc、p53、bax、bcl-2和caspase-3基因表达,并通过氧化应激,诱导HepG2细胞进入线粒体凋亡途径。

外文摘要：Objective： To investigate the mechanism of the apoptosis of HepG2 cells induced by total flavonoids from Broussonetia papyrifera. Methods： Effects of total flavonoids from Broussonetia papyrifera on cell cycle of HepG2 cells and intracellular reactive oxygen species （ROS） were detected by flow cytometry, the mRNA expressions of c-Myc, p53, bax, bcl-2 and caspase-3 related to tumor cell proliferation and apoptosis were determined by quantitative real-time PCR（ qRT-PCR）. Result： The proliferation of HepG2 cells was inhibited by total fla- vonoids from Broussonetia papyrifera supplement in dose-dependent manner. Treatment with 62.5 μg/ml of total flavonoids from Broussonetia papyrifera significantly inhibited the proliferation of HepG2 ceils. Flow cytometry analysis showed that 62.5 μg/ml of total flavonoids from Broussonetia papyrifera could significantly increase the apoptosis ratio of HepG2 ceils, which were accompanied with cell cycle arrested at G1 phase. Treatment with 200μg/ml of total flavonoids from Broussonetia papyrifera for 6 h significantly increased the intracellular ROS production of HepG2 cells. Moreover, the qRT-PCR analysis demonstrated that following the exposure to 100 μg/ml of total flavonoids from Brous- sonetia papyrifera for 24 h, the level of mRNA expression of p53, bax and caspase-3 of HepG2 cells were significantly up-regulated, whereas the expression of c-Myc and bcl-2 were down-regulated simultaneously. Conclusion ： The data obtained above revealed that c-Myc, p53, bax, bcl-2 and caspase-3 genes expressions of HepG2 cells were regulated by total flavonoids from Broussonetia papyrifera, and HepG2 cells apoptosis was induced via mitochondrial-mediated apoptosis pathway owing to intracellular oxidative stress.