Macrophage depletion ameliorates kavalactone damage in the isolated perfused rat liver
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- Zhang Lillian
- Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia
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- Rowe Anthony
- Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia
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- Braet Filip
- Australian Centre for Microscopy & Microanalysis, Madsen Building (F09), Camperdown Campus,University of Sydney,Australia
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- Ramzan Iqbal
- Faculty of Pharmacy, Pharmacy Bank Building (A15), Camperdown Campus, University of Sydney, Australia
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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.
収録刊行物
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- The Journal of Toxicological Sciences
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The Journal of Toxicological Sciences 37 (2), 447-453, 2012
一般社団法人 日本毒性学会
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詳細情報
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- CRID
- 1390001204903682944
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- NII論文ID
- 10030127153
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- NII書誌ID
- AN00002808
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- COI
- 1:CAS:528:DC%2BC38XotVylur0%3D
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- ISSN
- 18803989
- 03881350
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- NDL書誌ID
- 023674882
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- PubMed
- 22467036
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可