ID 72667
著者
フクハラ, ヤヨイ Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
土屋, 浩一郎 Department of Medical Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
ホリノウチ, ユウヤ Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧
タジマ, ソウイチロウ Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
木平, 孝高 Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
濱野, 修一 Department of Pathological Science and Technology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
川添, 和義 Department of Pharmacy, Tokushima University Hospital KAKEN研究者をさがす
池田, 康将 Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
石澤, 啓介 Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
冨田, 修平 Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
玉置, 俊晃 Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
nifedipine
nitrosonifedipine
antioxidant
tumor necrosis factor-α
reactive oxygen species
endothelial cells
cumene hydroperoxide
資料タイプ
学術雑誌論文
抄録
Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
58
1-2
開始ページ
118
終了ページ
126
並び順
118
発行日
2011-02
備考
The journal of medical investigation : http://medical.med.tokushima-u.ac.jp/jmi/index.html
EDB ID
フルテキストファイル
言語
eng
部局
薬学系
医学系