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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Author(s)

    • MORI Saori
    • Shimizu Research Laboratories, Reseach and Development Division, Shimizu Pharmaceutical Co., Ltd.
    • SATO Kazunori
    • Shimizu Research Laboratories, Reseach and Development Division, Shimizu Pharmaceutical Co., Ltd.
    • DOHI Sekiko
    • Shimizu Research Laboratories, Reseach and Development Division, Shimizu Pharmaceutical Co., Ltd.
    • SATO Takashi
    • Shimizu Research Laboratories, Reseach and Development Division, Shimizu Pharmaceutical Co., Ltd.
    • MATSUURA Akihiro
    • Shimizu Research Laboratories, Reseach and Development Division, Shimizu Pharmaceutical Co., Ltd.

Abstract

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<sup>−</sup><sup>1</sup> · h<sup>−</sup><sup>1</sup>) 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.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 89(1), 36-43, 2002-05-01

    The Japanese Pharmacological Society

References:  23

Cited by:  1

Codes

  • NII Article ID (NAID)
    10008430961
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    00215198
  • NDL Article ID
    6169337
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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