Effect of Raddeanin A on Proliferation and Apoptosis of Human Colon Cancer HT-29 Cells

被引:0
|
作者
Cui, Jinjie [1 ]
Zhao, Bo [1 ]
Yu, Sanshui [1 ]
Li, Zhulin [1 ]
Yang, Xinqing [1 ]
Zheng, Yi [1 ]
机构
[1] Capital Med Univ, Dept Gen Surg, Beijing Chaoyang Hosp, Beijing 100020, Peoples R China
来源
LATIN AMERICAN JOURNAL OF PHARMACY | 2019年 / 38卷 / 08期
关键词
apoptosis; colon cancer; HT-29; proliferation; raddeanin A; CHEMOTHERAPY; CASPASE-3; GROWTH; RISK;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
This study aimed to investigate the inhibitory effect of Raddeanin A (RA) on the proliferation and apoptosis of human colon cancer HT-29 cells and the possible mechanisms. HT-29 cells were cultured and treated with RA with concentration of 0 (control), 1, 2, 4, 8, and 16 mg/L. After treatment for 24, 48, and 72 h, the cell proliferation was determined, respectively. After treatment for 48 h, the cell apoptosis and cycle were detected. The expressions of B-cell lymphoma-2 (Bcl-2), B-cell lymphoma-2 associated X (Bax), cleaved cysteine aspartic acid specific protease-3 (cleaved caspase-3), extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphorylated extracellular signal-regulated kinase 1/2 (P-ERK1/2) protein were determined. Results showed that, RA could inhibit the proliferation of HT-29 cells, promote their apoptosis, and arrest most cells in G0/G1 phase. After treatment with RA, the expression level of Bcl-2 protein in HT-29 cells was decreased, the expression levels of Bax and Caspase-3 protein were increased, and the expression levels of ERK1/2 and P-ERK1/2 protein were decreased. In conclusion, RA has inhibitory effect on the growth of HT-29 cells, and the mechanism may be related to its inhibition of MAPK/ERK signaling pathway.
引用
收藏
页码:1663 / 1667
页数:5
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