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Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver

  • Zhang Lillian
    Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia
  • Rowe Anthony
    Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia
  • Braet Filip
    Australian Centre for Microscopy & Microanalysis, Madsen Building (F09), Camperdown Campus,University of Sydney,Australia
  • Ramzan Iqbal
    Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia

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Abstract

Liver toxicity is a side effect observed with some herbal treatments, including Piper methysticum. The possible mechanisms responsible include inflammation subsequent to activation of liver macrophages and oxidative damage. Hepatotoxicity of the pharmacologically active component of Piper methysticum (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 Piper methysticum. Characterisation and modulation of the liver macrophage response may enable the development of strategies to avoid these hepatic side effects.

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