Protective Effects of Peony Root Extract and Its Components on Neuron Damage in the Hippocampus Induced by the Cobalt Focus Epilepsy Model

Protective effects of peony root extract and its components on neuron damage in the CA1 area of the hippocampus induced by the cobalt focus epilepsy model were examined. Neuron damage in the CA1 area of the hippocampus and frequent spike discharges induced by application of metallic cobalt to the ce...

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Bibliographic Details
Published in:Experimental neurology 1997-08, Vol.146 (2), p.518-525
Main Authors: Tsuda, Tadashi, Sugaya, Aiko, Ohguchi, Hiromi, Kishida, Naoki, Sugaya, Eiichi
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cobalt
Electroencephalography
Epilepsy - chemically induced
Epilepsy - pathology
Epilepsy - physiopathology
Hippocampus - drug effects
Hippocampus - pathology
Medical sciences
Neurons - drug effects
Neurons - pathology
Neuropharmacology
Neuroprotective agent
Neuroprotective Agents - pharmacology
Pharmacology. Drug treatments
Plant Extracts - chemistry
Plant Extracts - pharmacology
Rats
Rats, Wistar
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Summary:Protective effects of peony root extract and its components on neuron damage in the CA1 area of the hippocampus induced by the cobalt focus epilepsy model were examined. Neuron damage in the CA1 area of the hippocampus and frequent spike discharges induced by application of metallic cobalt to the cerebral cortex of rats were completely prevented when peony root extract was continuously administered orally at 1 g/kg/day for 30 days prior to cobalt application. Component crude gallotannin fraction showed marked but incomplete protective action. A combination of crude gallotannin fraction and paeoniflorin showed complete protective action in the same way as peony root extract against neuron damage although use of paeoniflorin alone had no effect. These findings together with our previous reports indicate that peony root extract and its component, gallotannin, have excellent protective effects on neuron damage in addition to anticonvulsant action by prior oral administration.
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.1997.6570