Coptisine induces apoptosis in non-small cell lung cancer NCI-H1650 cells through ROS-dependent mito-chondria pathway
10.3969/j.issn.1006-5725.2017.24.004
- VernacularTitle: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
- Author:
Fan YANG
1
;
Xin LI
;
Tingting ZHANG
;
Jianrong LI
;
Yihua ZHU
;
Yahui HU
;
Hua LIU
Author Information
1. 443002,湖北省宜昌市第二人民医院放化疗一科
- Keywords:
coptisine;
apoptosis;
ROS;
non-small cell lung cancer;
NCI-H1650 cells
- From:
The Journal of Practical Medicine
2017;33(24):4033-4037
- CountryChina
- Language:Chinese
-
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.
