Chen Y.-N.TUR-FU HUANGChang C.-H.Hsu C.-C.Lin K.-T.Wang S.-W.Peng H.-C.Chung C.-H.2021-05-312021-05-312012218561https://scholars.lib.ntu.edu.tw/handle/123456789/564122The 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 β, mitogen-activated protein kinases, phosphoinositide 3-kinase/Akt, and phopholipase Cγ/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. ? 2012 American Chemical Society.[SDGs]SDG3butein; migration; PDGF; Restenosis; Smooth muscle cells; Phosphorylation; Diseases; butein; chalcone derivative; mitogen activated protein kinase; platelet derived growth factor; protein kinase B; animal; article; cell culture; cell motion; cell proliferation; cytology; drug effect; genetics; human; male; metabolism; neointima; pathophysiology; phosphorylation; rat; restenosis; signal transduction; smooth muscle fiber; Wistar rat; Animals; Cell Movement; Cell Proliferation; Cells, Cultured; Chalcones; Coronary Restenosis; Humans; Male; Mitogen-Activated Protein Kinases; Myocytes, Smooth Muscle; Neointima; Phosphorylation; Platelet-Derived Growth Factor; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Signal Transduction; Rattusjournal article10.1021/jf300771x226907542-s2.0-84863951045