Sanguinarine promotes apoptosis of HepG2 cells by inducing ROS
10.3969/j.issn.1001-1978.2018.03.015
- VernacularTitle:血根碱通过诱导活性氧促进HepG2细胞凋亡的机制研究
- Author:
Yi-Xuan YANG
1
;
Wen-Jing GUO
;
Cheng-Xu MA
;
Hai-Yan SU
;
Peng SONG
Author Information
1. 甘肃中医药大学附属医院检验科
- Keywords:
sanguinarine;
HepG2 cells;
ROS;
apop-tosis;
hepatic carcinoma;
signaling pathway
- From:
Chinese Pharmacological Bulletin
2018;34(3):370-375
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of sanguina-rine on regulating the pathway of cell apoptosis by in-ducing reactive oxygen species (ROS) in HepG2 cells. Methods MTT method was used to detect the cell viability of HepG2 cell after the treatment of san-guinarine. The changes of ROS were observed by indi-cator DCFH-DA and DHE staining. The apoptosis was detected by Hoechst 33342 and Annexin V/PI stai-ning;Rhodamine 123 staining was used to detect mito-chondrial membrane potential. Western blot was used to detect expressions of key cell-apoptotic protein. Re-sults The cell viability of HepG2 cells showed a de-creasing trend with the increasing concentration of san-guinarine. Sanguinarine could significantly increase cellular ROS,decrease mitochondrial membrane poten-tial in HepG2 cell, and promote apoptosis of HepG2 cells. The expression of Bax, cleaved-caspase-3 and cytoplasmic Cyt-C significantly increased after the treatment of sanguinarine, however, the expression of Bcl-2 was inhibited. Conclusion Sanguinarine could activate mitochondrial pathway of apoptosis mediated by cellular uncontrolled ROS and promote apoptosis of HepG2 cells.