Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/23310
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    標題: Lercanidipine inhibits vascular smooth muscle cell proliferation and neointimal formation via reducing intracellular reactive oxygen species and inactivating Ras-ERK1/2 signaling.
    作者: Jiunn-Ren Wu
    Shu-Fen Liou
    Shin-Wha Lin
    Chee-Yin Chai
    Zen-Kong Dai
    Jyh-Chong Liang
    Ing-Jun Chen
    Jwu-Lai Yeh
    貢獻者: 藥學系
    關鍵字: Lercanidipine
    Vascular smooth muscle cell
    Platelet-derived growth factor
    MAP kinase
    Reactive oxygen species
    日期: 2009-01
    上傳時間: 2010-12-29 15:05:21 (UTC+8)
    出版者: Academic Press Ltd Elsevier Science Ltd
    摘要: Lercanidipine, a calcium channel antagonist, is currently employed in the treatment of essential hypertension and angina pectoris. The purpose of this study was to elucidate the anti-proliferative effect of lercanidipine and to investigate the molecular role of this agent. Both in vitro studies and in a balloon injury rat carotid artery model were employed to study the effect of lercanidipine on smooth muscle cell proliferation. Lercanidipine-inhibited rat vascular smooth muscle cell (VSMC) proliferation and migration in a dose-dependent manner following stimulation of VSMC cultures with 10% fetal bovine serum (FBS) and 20 ng/ml platelet-derived growth factor (PDGF)-BB. FBS- and PDGF-BB-stimulated intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen (PCNA), and Akt activations were significantly inhibited by lercanidipine; however, lercanidipine did not affect FBS- and PDGF-BB-induced STAT3 phosphorylation. Lercanidipine also inhibited PDGF-receptor β chain phosphorylation and reactive oxygen species (ROS) production induced by PDGF-BB. Lercanidipine blocked the FBS-inducible progression through the G0/G1 to the S-phase of the cell cycle in synchronized cells. In vivo, 14 days after balloon injury, treatment with 3 and 10 mg/kg lercanidipine resulted in significant inhibition of the neointima/media ratio. Suppression of neointima formation by lercanidipine was dependent on its influence on ERK1/2 phosphorylation. These results demonstrate that lercanidipine can suppress the proliferation of VSMCs via inhibiting cellular ROS, Ras-MEK1/2-ERK1/2, and PI3K-Akt pathways, and suggesting that it may have therapeutic relevance in the prevention of human restenosis.
    關聯: Pharmacological Research 59(1):p.48-56
    顯示於類別:[藥學系(所)] 期刊論文

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