A Selective Thromboxane A2 (TXA2) Synthase Inhibitor, Ozagrel, Attenuates Lung Injury and Decreases Monocyte Chemoattractant Protein-1 and Interleukin-8 mRNA Expression in Oleic Acid-Induced Lung Injury in Guinea Pigs

  • Ishitsuka Yoichi
    Department of Clinical Chemistry and Informatics, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan
  • Moriuchi Hiroshi
    Laboratory of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Sojo University, Japan
  • Isohama Yoichiro
    Department of Chemico-Pharmacological Sciences, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan
  • Tokunaga Hidehiro
    Department of Surgical Pathology, Kumamoto University Hospital, Japan
  • Hatamoto Keita
    Department of Clinical Chemistry and Informatics, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan
  • Kurita Sumika
    Department of Clinical Chemistry and Informatics, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan
  • Irikura Mitsuru
    Department of Clinical Chemistry and Informatics, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan
  • Iyama Ken-ichi
    Department of Surgical Pathology, Kumamoto University Hospital, Japan
  • Irie Tetsumi
    Department of Clinical Chemistry and Informatics, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan

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This study examined the effect of ozagrel, a thromboxane A2 synthase inhibitor, on the accumulation of leucocytes and chemokine mRNA expression in lungs experimentally injured using oleic acid (OA). OA injection into guinea pigs rapidly increased thromboxane A2 generation and subsequently increased total protein concentration and the numbers of macrophages and neutrophils in bronchoalveolar lavage fluid and increased monocyte chemoattractant protein-1 and interleukin-8 mRNA expression in the whole lung. Administration of ozagrel prevented these changes associated with OA injection. Ozagrel is a promising drug candidate for preventing acute lung injury.<br>

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