916 research outputs found

    Alterations of [3H]Forskolin Binding in the Postischemic Rat Brain

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    開始ページ、終了ページ: 冊子体のページ付

    Development of a New in vivo Double Autoradiogram for the Analysis of Dopaminergic System of the Rat Brain

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    開始ページ、終了ページ: 冊子体のページ付

    Effect of Mergocriptine on Ischemia-induced Brain Damages

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    開始ページ、終了ページ: 冊子体のページ付

    Postischemic Changes of Spirodecanone Binding in the Gerbil Hippocampus

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    開始ページ、終了ページ: 冊子体のページ付

    Exo-Focal Postischemic Neuronal Death in the Rat Brain

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    開始ページ、終了ページ: 冊子体のページ付

    Inhibitory effect of ferulic acid and isoferulic acid on the production of macrophage inflammatory protein-2 in response to respiratory syncytial virus infection in RAW264.7 cells.

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    We investigated the effect of ferulic acid (FA) and isoferulic acid (IFA), which are the main active components of the rhizoma of Cimicifuga heracleifolia (CH), an anti-inflammatory drug used frequently in Japanese traditional medicine, on the production of macrophage inflammatory protein-2 (MIR-2) in a murine macrophage cell line, RAW264.7, in response to respiratory syncytial virus (RSV) infection. Following the exposure of cells to RSV for 20h, the MIP-2 level in condition medium was increased to about 20 ng/ml, although this level in mock-infected cells was negligible. In the presence of either FA or IFA, RSV-infected cells reduced MIP-2 production in a dose-dependent manner. These data suggest that FA and IFA might be responsible, at least in part, for the anti-inflammatory drug effect of CH extract through the inhibition of MIP-2 production

    Administration of isoferulic acid improved the survival rate of lethal influenza virus pneumonia in mice.

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    BACKGROUND: Isoferulic acid (IFA) is a main active ingredient of the rhizoma of Cimicifuga beracleifolia, which is used frequently in Japanese traditional medicine as an anti-inflammatory drug. It has been revealed that IFA inhibits the production of macrophage inflammatory protein-2 (MIP-2), which is a murine counterpart of the chemokine family that may contribute to the pathogenesis of inflammatory diseases through the chemotactic activity for inflammatory and immune effector cells. AIM OF THE STUDY: In this study, we investigated the therapeutic effect of IFA on the progression of lethal influenza virus pneumonia in mice by comparison with that of dexamethasone (DX), a potent inhibitor for various inflammatory cytokines including MIP-2. METHODS: Mice were infected by intranasal inoculation of influenza virus under ether anesthesia. The IFA or DX was given by oral administration once daily for 4 days after infection. After infection, the survival rate and the change in body weight were daily monitored. RESULTS: IFA administration markedly improved the survival rate and body weight loss of influenza virus-infected mice in a suitable dose range (0.5 mg/day). However, DX administration did not show a beneficial effect at any dose. CONCLUSION: These data suggested that IFA is a novel tool not only for the intervention therapy, but also for the studies on the pathogenesis of influenza virus-induced pneumonia
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