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学科主题: 药学
题名:
Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways
作者: Li, Ying-Bo1,2; Gao, Jian-Li3,4; Zhong, Zhang-Feng1; Hoi, Pui-Man1; Lee, Simon Ming-Yuen1; Wang, Yi-Tao1
关键词: Rhizoma Curcumae Longae ; bisdemethoxycurcumin (BDMC) ; reactive oxidative species (ROS) ; breast cancer
刊名: PHARMACOLOGICAL REPORTS
发表日期: 2013-05-01
卷: 65, 期:3, 页:700-709
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy
研究领域[WOS]: Pharmacology & Pharmacy
关键词[WOS]: CANCER-CELLS ; DOWN-REGULATION ; CURCUMIN ; APOPTOSIS ; THERAPY ; P53 ; DEMETHOXYCURCUMIN ; STRESS ; CHEMOPREVENTION ; DERIVATIVES
英文摘要:

Background: Bisdemethoxycurcumin (BDMC) is a natural derivative of curcumin present in the phenolic components extracted from the dried rhizome of Curcuma longa L. BDMC demonstrated potential chemotherapeutic activities but the underlying mechanisms have not been fully clarified. In the present stud, the role of reactive oxidative species (ROS) in the anti-cancer effects of BDMC was investigated.

Methods: MCF-7 cells were exposed to BDMC, and then the cell proliferation, colony formation ability and cell cycle profile were analyzed. Cellular ROS level was determined by flow cytometry and fluorescent microscope Observation using specific fluorescent probes. Mitochondrial membrane potential (psi m) was assessed using JC-1. In addition, effects of BDMC on senescence-related molecules were analyzed by western blot assay.

Results: BDMC significantly inhibited MCF-7 breast cancer cell proliferation, while a rapid rise of the intracellular ROS level accompanied with a reduction of Delta psi m were observed. In addition, BDMC activated the pro-apoptotic protein p53 and its downstream effector p21 as well as the cell cycle regulatory proteins p16 and its downstream effector retinoblastoma protein (Rb). All of these BDMC-induced effects were counteracted with the pre-incubation of the antioxidant N-acetylcysteine (NAC).

Conclusions: These results suggested that BDMC-induced ROS accumulation may contribute to its inhibitory effect on MCF-7 cell viability through regulation of p53/p21 and p16/Rb pathways.

语种: 英语
所属项目编号: 029/2007/A2
项目资助者: Macao Science and Technology Development Fund
WOS记录号: WOS:000330270400018
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54671
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Taipa 999078, Peoples R China
2.Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
3.Univ Chicago, Med Ctr, Mol Oncol Lab, Chicago, IL 60637 USA
4.Zhejiang Chinese Med Univ, Inst Mat Med, Hangzhou 310053, Zhejiang, Peoples R China

Recommended Citation:
Li, Ying-Bo,Gao, Jian-Li,Zhong, Zhang-Feng,et al. Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways[J]. PHARMACOLOGICAL REPORTS,2013,65(3):700-709.
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