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

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Author(s)

    • Fukuhara Yayoi
    • 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
    • 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
    • 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

Abstract

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

Journal

  • The Journal of Medical Investigation

    The Journal of Medical Investigation 58(1,2), 118-126, 2011

    The University of Tokushima Faculty of Medicine

Codes

  • NII Article ID (NAID)
    130004465233
  • Text Lang
    ENG
  • ISSN
    1343-1420
  • Data Source
    J-STAGE 
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