title: Cognitive dysfunctions induced by a cholinergic blockade and Aβ 25-35 peptide are attenuated by salvianolic acid B.
abstract: Alzheimer's disease (AD) is a neurodegenerative disorder associated with progressive cognitive and memory loss and neuronal cell death. Current therapeutic strategies for AD are very limited; thus, traditional herbal medicines or their active constituents receive much attention. The aim of this study was to investigate the cognitive enhancing effects of salvianolic acid B (SalB) isolated from Salvia miltiorrhiza and its ameliorating effects on various drug-induced amnesic models using the passive avoidance, Y-maze, and Morris water maze tasks. Drug-induced amnesia was induced by administering scopolamine, diazepam, muscimol, or amyloid-β (Aβ)(25-35) peptide. SalB (10 mg/kg, p.o.) was found to significantly reverse the cognitive impairments induced by scopolamine (1 mg/kg, i.p.) or Aβ(25-35) (10 nmol/5 μl, i.c.v.) injection. This ameliorating effect of SalB was antagonized by the GABA(A) receptor agonists, muscimol or diazepam, respectively. In addition, SalB alone was capable of improving cognitive performances. Furthermore, SalB (100 μM) was found to inhibit GABA-induced outward Cl(-) currents in single hippocampal CA1 neuron. These results suggest that the observed ameliorations of cholinergic dysfunction- or Aβ(25-35)-induced memory impairment by SalB were mediated, in part, via the GABAergic neurotransmitter system after a single administration.
authors: Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, Hoeki-dong, Dongdaemoon-Ku, Seoul 130-701, South Korea.
authors: Dong Hyun
authors: DH
authors: Kim
authors: Se Jin
authors: SJ
authors: Park
authors: Jong Min
authors: JM
authors: Kim
authors: Su Jin
authors: SJ
authors: Jeon
authors: Dae-Hoon
authors: DH
authors: Kim
authors: Young-Wuk
authors: YW
authors: Cho
authors: Kun Ho
authors: KH
authors: Son
authors: Hyoung Jae
authors: HJ
authors: Lee
authors: Jae-Hak
authors: JH
authors: Moon
authors: Jae Hoon
authors: JH
authors: Cheong
authors: Kwang Ho
authors: KH
authors: Ko
authors: Jong Hoon
authors: JH
authors: Ryu
mesh_terms: D016229:Amyloid beta-Peptides / Q000009:adverse effects*; D000818:Animals; D000831:Animals, Newborn; D001572:Benzofurans / Q000737:chemistry / Q000627:therapeutic use*; D018680:Cholinergic Antagonists / Q000009:adverse effects*; D002800:Cholinesterase Inhibitors / Q000009:adverse effects; D003072:Cognition Disorders / Q000139:chemically induced* / Q000188:drug therapy*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D006624:Hippocampus / Q000166:cytology; D066298:In Vitro Techniques; D007276:Injections, Intraventricular; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009474:Neurons / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010446:Peptide Fragments / Q000009:adverse effects*; D011247:Pregnancy; D051381:Rats; D013619:Tacrine / Q000009:adverse effects; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology; D053630:Depsides
chemical_list: D016229:Amyloid beta-Peptides; D001572:Benzofurans; D018680:Cholinergic Antagonists; D002800:Cholinesterase Inhibitors; D010446:Peptide Fragments; D013619:Tacrine; D005680:gamma-Aminobutyric Acid; C074636:amyloid beta-protein (25-35); C076944:salvianolic acid B; D053630:Depsides