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KAKEN_24790820seika.pdf
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Title |
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タバコ煙の肺胞上皮障害に対するスタチンの効果と作用機序
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Kana |
タバコエン ノ ハイホウ ジョウヒ ショウガイ ニ タイスル スタチン ノ コウカ ト サヨウ キジョ
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Tabakoen no haiho johi shogai ni taisuru sutachin no koka to sayo kijo
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The effect on the alveolar epitherial cell proliferation suppressed by cigarette smoking of simvastatin
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中鉢, 正太郎
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チュウバチ, ショウタロウ
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Chubachi, Shotaro
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慶應義塾大学・医学部・助教
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Research team head
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科研費研究者番号 : 90464867
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2014
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科学研究費補助金研究成果報告書
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2013
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HMG-CoA 還元酵素阻害剤(スタチン)は多面的作用を有する薬剤であり、COPD の病態を改善する可能性が指摘されてきた。我々はエラスターゼ誘導マウス肺気腫モデルにおいてスタチンが肺胞上皮細胞の再生亢進を促し、気腫化を抑制すること,短期喫煙マウスでの肺胞上皮細胞の増殖促進効果を報告している。本研究では肺胞上皮細胞に対するCSEの増殖抑制、スタチンの回復効果を確認した。またVEGFシグナリングの関与をin vitro、in vivoで検討した。
Statins exert pleiotropic effects, such as anti-inflammatory activity and improvement of endothelial cell function. We have previously reported that simvastatin inhibited the development of elastase-induced pulmonary emphysema in mice and also promoted the proliferation of alveolar epithelial cells in the lungs following cigarette-smoke exposure for 5 days, although the underlying mechanisms remain to be clarified. In this reserch, we examined the proliferative effects of simvastatin. CSE exposure significantly decreased the rate of cell proliferation. Pretreatment of A549 cells with simvastatin restored the proliferation at various concentrations in the presence of CSE. Interestingly, the effect of simvastatin to restore the cell proliferation was abolished by VEGF receptor blockade with SU5614, implying the endogenous VEGF signaling is involved in the mechanism. We also examined in vivo.
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研究種目 : 若手研究(B)
研究期間 : 2012~2013
課題番号 : 24790820
研究分野 : 医歯薬学
科研費の分科・細目 : 内科系臨床医学・呼吸器内科学
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