Differential Effects of Buckwheat and Kudingcha Extract on Neuronal Damage in Cultured Hippocampal Neurons and Spatial Memory Impairment Induced by Scopolamine in an Eight-Arm Radial Maze

  • Pu Fengling
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Mishima Kenichi
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Irie Keiichi
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Egashira Nobuaki
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Ishibashi Daisuke
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Matsumoto Yoshiaki
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Ikeda Tomoaki
    Department of Obstetrics and Gynecology, Miyazaki Medical College, University of Miyazaki
  • Iwasaki Katsunori
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
  • Fujii Hajime
    Amino Up Chemical Co., Ltd.
  • Kosuna Kenichi
    Amino Up Chemical Co., Ltd.
  • Fujiwara Michihiro
    Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University

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We have reported the neuroprotection provided by an extract of buckwheat (BWE, Fagopyrum esculentum Moench) on neuronal damage in the repeated cerebral ischemia model and demonstrated that BWE inhibited the excess glutamate release induced by repeated cerebral ischemia, suggesting that BWE had a free radical-scavenging in addition to anti-glutamate action. In the present study, we studied the neuroprotective effects of Kudingcha extract (KDE, Ligustrum purpurascens Y. C.) on scavenging by the 2,2-diphenyl-1-picylhydrazyl (DPPH) radical in primary cultured hippocampal neurons, and on spatial memory impairment induced by scopolamine in an eight-arm radial maze in comparison with BWE. The effects of KDE (0.01-1 mg/ml) were more potent than those of BWE (0.01-1 mg/ml) in scavenging the DPPH radical (1 mM). KDE (100 μg/ml) prevented the cell damage induced by glutamate (300 μM) or kainate (1 mM), which was more potent than BWE (100 μg/ml), but BWE suppressed the cellular damage induced by β-amyloid(25-35) (20 μM) more potently than KDE (100 μg/ml). BWE (600 mg/kg), but not KDE, significantly suppressed the increase in errors induced by scopolamine (0.5 mg/kg i.p.) in the eight-arm radial maze. The results suggest that BWE may protect against cholinergic dysfunction and that KDE protects more effectively against glutaminergic dysfunction. <br>

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