Antirestenosis Effect of Butein in the Neointima Formation Progression

被引:11
作者
Chen, Yen-Nien [1 ]
Huang, Tur-Fu [2 ]
Chang, Chien-Hsin [2 ]
Hsu, Chun-Chieh [2 ]
Lin, Kung-Tin [2 ]
Wang, Shih-Wei [3 ]
Peng, Hui-Chin [2 ]
Chung, Ching-Hu [1 ]
机构
[1] Tzu Chi Univ, Dept Pharmacol, Hualien, Taiwan
[2] Natl Taiwan Univ, Coll Med, Inst Pharmacol, Taipei, Taiwan
[3] Mackay Med Coll, Dept Med, New Taipei City, Taiwan
关键词
butein; smooth muscle cell; PDGF; restenosis; migration; VASCULAR SMOOTH-MUSCLE; GROWTH-FACTOR; INTIMAL HYPERPLASIA; CELL-PROLIFERATION; MIGRATION; KINASE; INJURY; PDGF; INHIBITION; ACTIVATION;
D O I
10.1021/jf300771x
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
The development of restenosis involves migration and hyperproliferation of vascular smooth muscle cells (VSMCs). Platelet-derived growth factor (PDGF) is one of the major factors. Butein modulates inflammatory pathways and affects the proliferation and invasion of the tumor. We investigated the hypothesis that butein might prevent the restenosis process via a similar pathway. Our results demonstrated that butein inhibited PDGF-induced VSMC proliferation and migration as determined by BrdU proliferation and two-dimensional migration scratch assay. Butein also concentration-dependently repressed PDGF-induced phosphorylation of PDGF-receptor beta, mitogen-activated protein kinases, phosphoinositide 3-kinase/Akt, and phopholipase C gamma/c-Src in VSMCs. In addition, in vivo results showed that butein attenuated neointima formation in balloon-injured rat carotid arteries. These results indicate that butein may inhibit PDGF-induced VSMC proliferation and migration, resulting in attenuation of neointima formation after percutaneous transluminal coronary angioplasty. Our study demonstrates for the first time that systemic administration of butein is able to reduce neointima formation after vascular injury.
引用
收藏
页码:6832 / 6838
页数:7
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