Neuroprotective effects of salvianolic acid B on an Aβ25–35 peptide-induced mouse model of Alzheimer's disease

Salvianolic acid B (SalB) is a polyphenolic compound found in Salvia miltiorrhiza Bunge that has several anti-oxidative and anti-inflammatory effects. In the present study, we investigated whether SalB has neuroprotective effects in an amyloid β (Aβ) peptide-induced Alzheimer's disease mouse mo...

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Veröffentlicht in:	European journal of pharmacology 2013-03, Vol.704 (1-3), p.70-77
Hauptverfasser:	Lee, Young Woo, Kim, Dong Hyun, Jeon, Su Jin, Park, Se Jin, Kim, Jong Min, Jung, Jun Man, Lee, Hyung Eun, Bae, Shin Gil, Oh, Hee Kyong, Ho Son, Kun Ho, Ryu, Jong Hoon
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Amyloid beta-Peptides Amyloid β protein Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Avoidance Learning - drug effects Behavior, Animal - drug effects Benzofurans - pharmacology Benzofurans - therapeutic use Brain-Derived Neurotrophic Factor - metabolism Choline O-Acetyltransferase - metabolism Cognition Disorders - drug therapy Cognition Disorders - metabolism Cognition Disorders - physiopathology Cyclooxygenase 2 - metabolism Disease Models, Animal Hippocampus - cytology Hippocampus - drug effects Hippocampus - metabolism Lipid Peroxidation - drug effects Male Mice Mice, Inbred ICR Neuroglia - drug effects Neuroglia - metabolism Neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Nitric Oxide Synthase Type II - metabolism Peptide Fragments Salvianolic acid B
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Beschreibung
Zusammenfassung:	Salvianolic acid B (SalB) is a polyphenolic compound found in Salvia miltiorrhiza Bunge that has several anti-oxidative and anti-inflammatory effects. In the present study, we investigated whether SalB has neuroprotective effects in an amyloid β (Aβ) peptide-induced Alzheimer's disease mouse model. Mice were injected with Aβ25–35 peptide intracerebroventricularly and were subsequently administered SalB once daily for 7 days. Subchronic SalB administration (10mg/kg) significantly ameliorated the Aβ25–35 peptide-induced memory impairment in the passive avoidance task (P
ISSN:	0014-2999 1879-0712
DOI:	10.1016/j.ejphar.2013.02.015