Salicin, an Extract from White Willow Bark, Inhibits Angiogenesis by Blocking the ROS-ERK Pathways

被引:24
|
作者
Kong, Chang-Seok [1 ]
Kim, Ka-Hyun [2 ]
Choi, Jae-Sun [1 ,4 ]
Kim, Ja-Eun [1 ,3 ]
Park, Chan [1 ,4 ]
Jeong, Joo-Won [1 ,2 ,4 ]
机构
[1] Kyung Hee Univ, Inst Biomed Sci, Sch Med, Dept Biomed Sci, Seoul 130701, South Korea
[2] Kyung Hee Univ, Inst Biomed Sci, Sch Med, Dept Neurosci, Seoul 130701, South Korea
[3] Kyung Hee Univ, Inst Biomed Sci, Sch Med, Dept Pharmacol, Seoul 130701, South Korea
[4] Kyung Hee Univ, Inst Biomed Sci, Sch Med, Dept Anat & Neurobiol, Seoul 130701, South Korea
基金
新加坡国家研究基金会;
关键词
salicin; angiogenesis; tumor progression; ROS; ERK; ENDOTHELIAL GROWTH-FACTOR; TUMOR ANGIOGENESIS; CELLS; EXPRESSION; CANCER; VEGF; PROLIFERATION; MODULATION; ACTIVATION; OXIDASE;
D O I
10.1002/ptr.5126
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Salicin has been studied as a potent antiinflammatory agent. Angiogenesis is an essential process for tumor progression, and negative regulation of angiogenesis provides a good strategy for antitumor therapy. However, the potential medicinal value of salicin on antitumorigenic and antiangiogenic effects remain unexplored. In this study, we examined the antitumorigenic and antiangiogenic activity of salicin and its underlying mechanism of action. Salicin suppressed the angiogenic activity of endothelial cells, such as migration, tube formation, and sprouting from an aorta. Moreover, salicin reduced reactive oxygen species production and activation of the extracellular signal-regulated kinase pathway. The expression of vascular endothelial growth factor was also decreased by salicin in endothelial cells. When the salicin was administered to mice, salicin inhibited tumor growth and angiogenesis in a mouse tumor model. Taken together, salicin targets the signaling pathways mediated by reactive oxygen species and extracellular signal-regulated kinase, providing new perspectives into a potent therapeutic agent for hypervascularized tumors. Copyright (c) 2014 John Wiley & Sons, Ltd.
引用
收藏
页码:1246 / 1251
页数:6
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