实用医学杂志2017，Vol.33Issue(24)：4033-4037,5.DOI:10.3969/j.issn.1006-5725.2017.24.004
黄连碱经活性氧中介物-线粒体途径诱导肺癌NCI-H1650细胞凋亡
Coptisine induces apoptosis in non-small cell lung cancer NCI-H1650 cells through ROS-dependent mito-chondria pathway
摘要
Abstract
Objective To explore the effect of coptisine on the growth of NCI-H1650cells and to evaluate its potential value in the treatment of human non-small cell lung cancer. Methods MTT method was used to ana-lyze cell proliferation. Protein expressions of Bax/Bcl-2 and cytochrome C in NCI-H1650 cells were detected by-Western blot.Apoptosis was analyzed using flow cytometrywithAnnexin V/PI method.ROS concentration was tested with fluorometry.Results Coptisine could significantly inhibit growth of NCI-H1650 cells in a time-and dose-de-pendent manner.Coptisine induced apoptosis in NCI-H1650 cells by inducing ROS accumulation and the following mitochondria mediated apoptosis which was identified by increased Bax expression,Bcl-2 expression was down-reg-ulated,and cytochrome C moved from mitochondria to cytoplasm.ROS inhibitor(N-acetyl cysteine)treatment dra-matically abrogated coptisine-induced growth inhibition and apoptosis.Conclusions This study suggests that copti-sine can induce ROS irritated-and mitochondria-mediated apoptosis in NCI-H1650 cells.Coptisine has a potential value in the treatment of human non-small cell lung cancer.关键词
黄连碱/细胞凋亡/活性氧中介物/非小细胞肺癌/NCI-H1650细胞Key words
coptisine/apoptosis/ROS/non-small cell lung cancer/NCI-H1650 cells引用本文复制引用
杨凡,李欣,章婷婷,李建荣,祝艺华,胡亚辉,刘华..黄连碱经活性氧中介物-线粒体途径诱导肺癌NCI-H1650细胞凋亡[J].实用医学杂志,2017,33(24):4033-4037,5.基金项目
宜昌市科技局公益类科技项目基金资助(编号:A16-301-29) （编号:A16-301-29）
