Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

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Liver toxicity is a side effect observed with some herbal treatments, including <i>Piper methysticum</i>. The possible mechanisms responsible include inflammation subsequent to activation of liver macrophages and oxidative damage. Hepatotoxicity of the pharmacologically active component of <i>Piper methysticum</i> (kavalactones) was tested in isolated, perfused livers from rats which were pretreated with the macrophage intoxicant gadolinium chloride. Perfusions without kavalactones in gadolinium chloride pretreated and untreated livers were included as negative controls. Serial liver lobe biopsies were collected to measure temporal changes in available (reduced) hepatic glutathione. There were no statistically significant changes in reduced glutathione over the course of perfusion in any experimental group. Liver damage was observed using electron microscopy. Hepatic sinusoids displayed extensive damage to the endothelium in kavalactone-perfused, rat livers. This damage was significantly reduced by pre-treatment with gadolinium chloride. Hence liver macrophages may be a factor in liver injury induced by <i>Piper methysticum</i>. Characterisation and modulation of the liver macrophage response may enable the development of strategies to avoid these hepatic side effects.

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  • Journal of toxicological sciences

    Journal of toxicological sciences 37(2), 447-453, 2012-04-01

    一般社団法人 日本毒性学会

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各種コード

  • NII論文ID(NAID)
    10030127153
  • NII書誌ID(NCID)
    AN00002808
  • 本文言語コード
    ENG
  • 資料種別
    OTR
  • ISSN
    03881350
  • NDL 記事登録ID
    023674882
  • NDL 請求記号
    Z19-1022
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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