Neuroprotective effect of Kampo medicine against brain ischemia and its mode of action
| Project/Area Number |
16590556
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General internal medicine (including Psychosomatic medicine)
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| Research Institution | University of Toyama (2005-2006)
Toyama Medical and Pharmaceutical University (2004) |
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Principal Investigator |
SHIMADA Yutaka University of Toyama, Graduate School of Medicine and Pharmaceutical Sciences, Professor, 医学薬学研究部(医学), 教授 (80251891)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Hirozo University of Toyama, Graduate School of Medicine and Pharmaceutical Sciences, Associate Professor, 医学薬学研究部(医学), 助教授 (40313598)
HIKIAMI Hiroaki University of Toyama, Graduate School of Medicine and Pharmaceutical Sciences, Assistant Professor, 医学薬学研究部(医学), 講師 (70345586)
関矢 信康 富山医科薬科大学, 医学部, 助手 (40345575)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Kampo medicine / neuroprotective effect / chotosan / Uncaria sinensis / 一過性脳虚血 / 一酸化窒素 / フリーラジカル / 抗酸化酵素 |
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| Research Abstract |
Previously, we have revealed that chotosan (Diao-teng-san), a Kampo formula, is effective on vascular dementia clinically, and the hooks and stems of Uncaria sinensis, a medicinal plant comprising chotosan, has a neuroprotective effect in vitro. For the purpose of clarifying their effects in vivo, we investigated whether the oral administration of chotosan extract (CSE) or Uncaria sinensis extract (USE) reduces delayed neuronal death of pyramidal cells in the hippocampus following ischemia/reperfusion (i/rp) in gerbils. CSE or USE were dissolved in drinking water and provided to the gerbils ad libitum from 7 days prior to i/rp until 7 days after i/rp. It was found that CSE-or USE-treatments significantly reduced pyramidal cell death in the hippocampal CA1 region at 7 days after i/rp. Lipid peroxide (LPO) and nitrite (NO_2^-)/nitrate (NO_3^-) levels of the hippocampus at 48 hr after i/rp in the CSE- or USE-treated groups were significantly lower than those of control. Superoxide anion (O_2^-・) and hydroxyl radical (HO・) scavenging activities in both the hippocampus and cortex without i/rp, and also at 3 hours and 7 days after i/rp, were enhanced by the administration of CSE or USE. Administrations of CSE or USE without i/rp procedure enhanced catalase (CAT) activity but not superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in both the hippocampus and cortex. CSE elevated CAT activity in the hippocampus at 7 days and that in the cortex at 3 hours after i/rp. USE raised CAT activity in both the hippocampus and cortex at 3 hours and 7 days after i/rp. These results suggest that the oral administrations of CSE and USE provide a protective effect against transient ischemia-induced delayed neuronal death by reducing oxidative damage to neurons, and one of the mechanisms may be their enhancing effect on CAT activity in the brain.
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Report
(4 results)
Research Products
(7 results)
