Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells

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  • Fukuhara Yayoi
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Tsuchiya Koichiro
    Department of Medical Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Horinouchi Yuya
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Tajima Soichiro
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Kihira Yoshitaka
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Hamano Shuichi
    Department of Pathological Science and Technology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Kawazoe Kazuyoshi
    Department of Pharmacy, Tokushima University Hospital
  • Ikeda Yasumasa
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Ishizawa Keisuke
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Tomita Shuhei
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School
  • Tamaki Toshiaki
    Department of Pharmacology, Institute of Health Bioscience, the University of Tokushima Graduate School

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説明

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. J. Med. Invest. 58: 118-126, February, 2011

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