Propofol Protects against Anandamide-Induced Injury in Human Umbilical Vein Endothelial Cells
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- ITO TAKAHIKO
- Department of Anesthesiology, Kurume University School of Medicine
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- MISHIMA YASUNORI
- Department of Anesthesiology, Kurume University School of Medicine
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- ITO ASUKA
- Department of Anesthesiology, Kurume University School of Medicine
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- KAMEYAMA NAOMITSU
- Department of Anesthesiology, Kurume University School of Medicine
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- HARADA HIDEKI
- Department of Anesthesiology, Kurume University School of Medicine
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- IWATA OSUKE
- Department of Pediatrics, Kurume University School of Medicine
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- WATANABE SEIJI
- Department of Anesthesiology, Kurume University School of Medicine
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- USHIJIMA KAZUO
- Department of Anesthesiology, Kurume University School of Medicine
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Endocannabinoid anandamide, arachidonylethanolamine (AEA), is considered to be a causative mediator of hemorrhagic or septic shock, inducing death of several types of cells by producing free radicals such as reactive oxygen species (ROS). Propofol contains a phenolic hydroxyl group that donates electrons to the free radicals, and thus functions as an antioxidant. The purpose of this study was to investigate the protective effect of propofol against AEA-induced cell injury. After incubation with propofol at concentrations of 10, 50 or 100 μM, human umbilical vein endothelial cells (HUVECs) were stimulated with 10 μM of AEA for 24 h. ROS production, caspase-3 activity, and cell viability were evaluated 1, 8, and 24 h after the administration of 10 μM of AEA, respectively. Propofol (50 μM) significantly attenuated cell death induced by AEA, showing a protective effect against ROS production and caspase-3 activity. These results suggest that propofol at concentrations used during clinical anesthesia protects HUVECs against AEA-induced injury, in part by suppressing apoptosis.
収録刊行物
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- The Kurume Medical Journal
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The Kurume Medical Journal 58 (1), 15-20, 2011
久留米大学医学部 The Kurume Medical Journal 編集部
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詳細情報 詳細情報について
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- CRID
- 1390001206344535168
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- NII論文ID
- 130001444130
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- ISSN
- 18812090
- 00235679
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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
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- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可