Effects of ginseng saponins on β-amyloid-induced amnesia in rats
| Autor: | Tze-Fun Lee, Sum-Yan Ng, Beatrice Wang, Lawrence C.H. Wang |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Male
medicine.medical_specialty Panax Amnesia Hippocampal formation Hippocampus Rats Sprague-Dawley chemistry.chemical_compound Ginseng In vivo Internal medicine mental disorders Drug Discovery medicine Animals Memory disorder Neurotransmitter Pharmacology Amyloid beta-Peptides Saponins medicine.disease Acetylcholine Frontal Lobe Rats Endocrinology chemistry Cholinergic medicine.symptom medicine.drug |
| Zdroj: | Journal of Ethnopharmacology. 103:103-108 |
| ISSN: | 0378-8741 |
| Popis: | We have previously demonstrated that ginseng saponins (GS) can reverse the inhibitory effect of beta-amyloid on acetylcholine (ACh) release in the hippocampal slices. The present study was carried out to examine whether GS has any beneficial effects against amnesia induced by beta-amyloid peptides in vivo. Intracerebroventricular injection of 50 microg, but not 10 microg, beta-amyloid fragment(25-35) markedly impaired the performance of rats in avoiding a shock prod, confirming the amnesiac effect of beta-amyloid. Chronically treating the rats with GS (orally, 5 days before icv beta-amyloid injection and 7 days afterward) resulted in a dose-related improvement against beta-amyloid-induced amnesia; a significant reversion was observed at the highest GS dose (80 mg/kg/day). Post-treatment analysis on K(+)-evoked [(3)H]-ACh release from the hippocampal slices showed that beta-amyloid-treatment significantly reduced ACh release from that of the control group. However, pre-treatment with GS completely protected the animal against beta-amyloid-induced reduction of hippocampal ACh release. In contrast, treating the animals with the same optimal dose of GS and duration but only after icv beta-amyloid injection was found to be ineffective in obliterating beta-amyloid's amnesiac effect. Taken together, these observations indicated that GS pre-treatment can functionally prevent the beta-amyloid-induced memory loss possibly by minimizing the inhibitory effect of beta-amyloid on hippocampal cholinergic transmission. |
| Databáze: | OpenAIRE |
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