Lansoprazole Inhibits Nitric Oxide and Prostaglandin E2 Production in Murine Macrophage RAW 264.7 Cells
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  • 作者:Shuji Nakagawa (1)
    Yuji Arai (1) yarai89046@nike.eonet.ne.jp
    Tsunao Kishida (2)
    Nobuyuki Hiraoka (1)
    Shinji Tsuchida (1)
    Hiroaki Inoue (1)
    Ryo Sakai (1)
    Osam Mazda (2)
    Toshikazu Kubo (1)
  • 关键词:KEY WORDS lansoprazole &#8211 ; macrophage &#8211 ; nitric oxide &#8211 ; prostaglandin E2 &#8211 ; NADPH oxidase
  • 刊名:Inflammation
  • 出版年:2012
  • 出版时间:June 2012
  • 年:2012
  • 卷:35
  • 期:3
  • 页码:1062-1068
  • 全文大小:197.8 KB
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  • 作者单位:1. Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566 Japan2. Department of Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566 Japan
  • 刊物类别:Medicine
  • 刊物主题:Medicine & Public Health
    Rheumatology
    Internal Medicine
    Pharmacology and Toxicology
    Pathology
  • 出版者:Springer Netherlands
  • ISSN:1573-2576
文摘
Aberrantly activated macrophages, which overproduce inflammatory mediators, are involved in the pathogenesis of many inflammatory diseases. We analyzed the anti-inflammatory activity of lansoprazole (LPZ), a typical proton pump (P-ATPase) inhibitor, on RAW264.7 murine macrophages. Treatment of lipopolysaccharide (LPS)-stimulated RAW264.7 cells with LPZ inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2). Since P-ATPase expression was not observed in RAW264.7 cells, the anti-inflammatory effect of LPZ was independent of ATPase. In contrast, diphenylene iodonium (DPI), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, decreased NO but not PGE2 levels. LPZ suppressed the LPS-stimulated production by RAW264.7 cells of reactive oxygen species (ROS), which plays an important role in inflammatory responses. ROS elevation in these cells was associated with NO but not PGE2 production, suggesting that LPZ inhibits NO production by suppressing NADPH oxidase activity. These findings suggest that LPZ may be useful in the treatment of many inflammatory diseases associated with activated macrophages.

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