Exploiting the Nephrotoxic Effects of Venom from the Sea Anemone, Phyllodiscus semoni, to Create a Hemolytic Uremic Syndrome Model in the Rat
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- Masashi Mizuno
- Renal Replacement Therapy, Division of Nephrology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
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- Yasuhiko Ito
- Renal Replacement Therapy, Division of Nephrology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
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- B. Paul Morgan
- Complement Biology Group, Institute of Infection and Immunology, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK
書誌事項
- 公開日
- 2012-07-23
- 資源種別
- journal article
- 権利情報
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- https://creativecommons.org/licenses/by/3.0/
- DOI
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- 10.3390/md10071582
- 公開者
- MDPI AG
説明
<jats:p>In the natural world, there are many creatures with venoms that have interesting and varied activities. Although the sea anemone, a member of the phylum Coelenterata, has venom that it uses to capture and immobilise small fishes and shrimp and for protection from predators, most sea anemones are harmless to man. However, a few species are highly toxic; some have venoms containing neurotoxins, recently suggested as potential immune-modulators for therapeutic application in immune diseases. Phyllodiscus semoni is a highly toxic sea anemone; the venom has multiple effects, including lethality, hemolysis and renal injuries. We previously reported that venom extracted from Phyllodiscus semoni induced acute glomerular endothelial injuries in rats resembling hemolytic uremic syndrome (HUS), accompanied with complement dysregulation in glomeruli and suggested that the model might be useful for analyses of pathology and development of therapeutic approaches in HUS. In this mini-review, we describe in detail the venom-induced acute renal injuries in rat and summarize how the venom of Phyllodiscus semoni could have potential as a tool for analyses of complement activation and therapeutic interventions in HUS.</jats:p>
収録刊行物
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- Marine Drugs
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Marine Drugs 10 (7), 1582-1604, 2012-07-23
MDPI AG
