Anti-proliferation of Angong Niuhuang pill on tumor cells via inducement of apoptosis and down-regulation of mitochondrial membrane potential
10.3867/j.issn.1000-3002.2012.03.003
- VernacularTitle:安宫牛黄丸通过诱导细胞凋亡和降低线粒体膜电位抑制肿瘤细胞增殖
- Author:
Zhikai DAI
;
Jiaoe HUANG
;
Jinyu JIANG
;
Hailu ZHAO
;
Yong LUO
- Publication Type:Journal Article
- Keywords:
Angong Niuhuang pill;
MGC-803 cells;
BEL-7402 cells;
cell proliferation;
apoptosis;
mitochondrial membrane potential
- From:
Chinese Journal of Pharmacology and Toxicology
2012;26(3):269-275
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To validate the anticancer effect of Angong Niuhuang pill (AGNH) and pinpoint associated molecular mechanisms using human cancer cells.METHODS Human MGC-803 gastric carcinoma and human BEL-7402 hepatocarcinoma cells were incubated with AGNH 9,30,90,300 and 900 mg·L-1 for 24,48and 72 h,respectively.Cell viability was detected with 3-(4,5-dimethylthiazol-2-yl) -5-( 3-carboxymethoxyphe-nyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and colony formation assay.Apoptosis was measured with flow cytometry and Hoechst 33258/PI staining.Change in mitochondrial membrane potential (△qψ) was detected by spectrofluorophotometer.RESULTS AGNH inhibited MGC-803 cell proliferation ( for 48 h,r =0.996,P =0.002; for72 h,r=0.756,P=0.024 ) and BEL-7402 cells (for 48 h,r =0.732,P=0.030; for72 h,r=0.702,P =0.037) in a concentration-dependent manner,as showed by MTS assay.AGNH inhibited colony formation on MGC-803 cells (r =0.914,P =0.011 ) and BEL-7402 cells (r =0.871,P =0.024) in a concentration-dependent manner for 24 h.Hoechst 33258/PI staining and flow cytometry assay showed that AGNH 900 mg·L-1 for 24 h induced apoptosis of MGC-803 and BEL-7402 cells,and the apoptosis rate was 27.2％ and 19.7％,respectively.Compared with normal control group,AGNH 900 mg·L-1 for 3 min decreased the mitochondrial membrane potential of MGC-803 and BEL-7402 cells to 15.9％ and 15.0％ of control group.CONCLUSION AGNH inhibits proliferation of human cancer cells.Apoptosis and depolarization of mitochondrial transmembrane potential are probablly its mechanism.
