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Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways
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
2013-05-01
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
WOS记录号WOS:000330270400018
项目编号029/2007/A2
资助机构Macao Science and Technology Development Fund
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54671
专题北京大学药学院
北京大学药学院_天然药物与仿生药物国家重点实验室
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
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GB/T 7714
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.
APA Li, Ying-Bo,Gao, Jian-Li,Zhong, Zhang-Feng,Hoi, Pui-Man,Lee, Simon Ming-Yuen,&Wang, Yi-Tao.(2013).Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways.PHARMACOLOGICAL REPORTS,65(3),700-709.
MLA Li, Ying-Bo,et al."Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways".PHARMACOLOGICAL REPORTS 65.3(2013):700-709.
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