β-Hydroxybutyrate, a Cerebral Function Improving Agent, Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral Ischemia
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- Suzuki Motohisa
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Suzuki Mayumi
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Kitamura Yukika
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Mori Saori
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Sato Kazunori
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Dohi Sekiko
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Sato Takashi
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Matsuura Akihiro
- Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.
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- Hiraide Atsushi
- Department of General Medicine, Osaka University Medical School
書誌事項
- タイトル別名
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- .BETA.-Hydroxybutyrate, a Cerebral Function Improving Agent, Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral Ischemia.
- ベータ Hydroxybutyrate a Cerebral Function Improving Agent Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral Ischemia
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抄録
In our previous study, β-hydroxybutyrate (BHB) was found to prolong survival time and to inhibit cerebral edema by improving energy metabolism in the hypoxia, anoxia and global cerebral ischemia models. In this study, the cerebroprotective effect of BHB was examined in rats with permanent (p)-occlusion and transient (t)-occlusion of middle cerebral artery (MCA). BHB (30 mg · kg−1 · h−1) was continuously administered through the femoral vein. In rats with p-MCA occlusion, BHB significantly reduced infarct area at 24 h after the occlusion, but not at 72 h after the occlusion. In rats with 2-h t-MCA occlusion followed by 22-h reperfusion, BHB significantly reduced cerebral infarct area, edema formation, lipid peroxidation and neurological deficits. Moreover, in the t-MCA occlusion model, delayed administration of BHB started at 1 h after the initiation of the MCA occlusion also significantly reduced cerebral infarct area. Taking together the results obtained in our previous study into account, these results indicate that BHB decreased cerebral edema formation and infarct area by improving of the cerebral energy metabolism during ischemia and by inhibition of lipid peroxidation after reperfusion.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 89 (1), 36-43, 2002
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204285991552
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- NII論文ID
- 10008430961
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- NII書誌ID
- AA00691188
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- COI
- 1:STN:280:DC%2BD38zktFSmtA%3D%3D
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- ISSN
- 13473506
- 00215198
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- NDL書誌ID
- 6169337
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- PubMed
- 12083741
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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