β-Hydroxybutyrate, a Cerebral Function Improving Agent, Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral Ischemia

The Japanese Journal of Pharmacology

Takashi Sato¹  Yukika Kitamura¹  Akihiro Matsuura¹  Atsushi Hiraide²  Motohisa Suzuki¹  Sekiko Dohi¹  Kazunori Sato¹  Saori Mori¹  Mayumi Suzuki¹ 

[1] Shimizu Research Laboratories, Research and Development Division, Shimizu Pharmaceutical Co., Ltd.;Department of General Medicine, Osaka University Medical School

关键词: β-Hydroxybutyrate;    Permanent ischemia;    Transient ischemia;    Middle cerebral artery occlusion;    Cerebroprotection;   

DOI  :  10.1254/jjp.89.36

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(23)Cited-By(49)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.

【 授权许可】

Unknown