Paeoniflorin inhibits growth of human colorectal carcinoma HT 29 cells in vitro and in vivo

被引:55
作者
Wang, He [1 ]
Zhou, Hong [2 ]
Wang, Cheng-Xi [3 ]
Li, Yue-Shan [1 ]
Xie, Hong-Yan [1 ]
Luo, Jian-Dong [1 ]
Zhou, Yi [1 ]
机构
[1] Guangzhou Med Univ, Dept Pharmaceut Sci, Guangzhou 510182, Guangdong, Peoples R China
[2] Guangdong Prov Tradit Chinese Med Hosp, Guangzhou 510140, Peoples R China
[3] So Med Univ, Nanfang Hosp, Dept Pharmaceut Sci, Guangzhou 510515, Guangdong, Peoples R China
关键词
Proliferation; HT29; cells; In vitro and in vivo; P53; Apoptosis; CYTOCHROME-C RELEASE; PAEONIA-LACTIFLORA; 14-3-3; PROTEINS; CANCER; APOPTOSIS; ACTIVATION; EXPRESSION; P53; PHOSPHORYLATION; EXTRACT;
D O I
10.1016/j.fct.2012.01.035
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The aim of the therapy of human malignancies is the inhibition of cell proliferation and/or induction of apoptosis. In present experiment, we investigated the in vitro and in vivo anticancer effects and associated mechanisms of paeoniflorin (PF), isolated from the paeony root, against colorectal cancer. In vitro, cell growth assay obviously showed the inhibition of tumor cell growth in a dose-dependent manner. Flow cytometry analysis showed that PF could mainly have the cell cycle arrest at G1, which is associated with DNA damage and activation of p53/14-3-3 zeta (zeta). The pro-apoptotic effect of PF was demonstrated by Annexin V-PI staining, and activation of caspase-3 and caspase-9 by Western immunoblotting. In vivo, the results showed that positive cells of PCNA in PF and docetaxel-treated group was decreased to 30% and 15% compared with control group of tumors, respectively. But apoptosis cells in PF- and docetaxel treated groups studied by TUNEL is increased to 40 +/- 1.2% and 30 +/- 1.5% compared with 24 +/- 2.3% in negative control, respectively. Furthermore, the efficiency of tumor-bearing mice treated by PF was superior to docetaxel in vivo. Overall. PF may be an effective chemopreventive agent against colorectal cancer HT29, and the mechanism could be mediated via an regulation of p53/14-3-3 zeta. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1560 / 1567
页数:8
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