ASIA unversity:Item 310904400/79717
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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79717


    Title: Anti-Neuroinflammatory Effects of the Calcium Channel Blocker Nicardipine on Microglial Cells: Implications for Neuroprotection
    Authors: Bor-Ren Huang;Pei-Chun Chang;Wei-Lan Yeh;Chih-Hao Lee;Cheng-Fang Tsai;Chingju Lin;Hsiao-Yun Lin;Yu-Shu Liu;Caren Yu-Ju Wu;Pei-Ying Ko;Shiang-Suo Huang;Horng-Chaung Hsu;Dah-Yuu Lu
    Contributors: 生物科技學系
    Date: 2014-03
    Issue Date: 2014-06-05 03:58:00 (UTC+0)
    Abstract: Background/Objective

    Nicardipine is a calcium channel blocker that has been widely used to control blood pressure in severe hypertension following events such as ischemic stroke, traumatic brain injury, and intracerebral hemorrhage. However, accumulating evidence suggests that inflammatory processes in the central nervous system that are mediated by microglial activation play important roles in neurodegeneration, and the effect of nicardipine on microglial activation remains unresolved.

    Methodology/Principal Findings

    In the present study, using murine BV-2 microglia, we demonstrated that nicardipine significantly inhibits microglia-related neuroinflammatory responses. Treatment with nicardipine inhibited microglial cell migration. Nicardipine also significantly inhibited LPS plus IFN-γ-induced release of nitric oxide (NO), and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, nicardipine also inhibited microglial activation by peptidoglycan, the major component of the Gram-positive bacterium cell wall. Notably, nicardipine also showed significant anti-neuroinflammatory effects on microglial activation in mice in vivo.

    Conclusion/Significance

    The present study is the first to report a novel inhibitory role of nicardipine on neuroinflammation and provides a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases.
    Relation: PLoS One,9(3): e91167.
    Appears in Collections:[Department of Biotechnology] Journal Article

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