Attenuation of scopolamine-induced cognitive dysfunction by obovatol

Title
Attenuation of scopolamine-induced cognitive dysfunction by obovatol
Author(s)
최동영이영중[이영중]이선영[이선영]이윷모[이윷모]이현희[이현희]최임섭[최임섭]오기완[오기완]한상배[한상배]남상윤[남상윤]홍진태[홍진태]
Keywords
AMYLOID PRECURSOR PROTEIN; FOREBRAIN CHOLINERGIC SYSTEM; INDUCED MEMORY IMPAIRMENTS; ALZHEIMERS-DISEASE; ACETYLCHOLINESTERASE ACTIVITY; CHOLINESTERASE-INHIBITORS; MAGNOLIA-OFFICINALIS; CEREBROSPINAL-FLUID; MUSCARINIC AGONIST; INDUCED AMNESIA
Issue Date
201207
Publisher
PHARMACEUTICAL SOC KOREA
Citation
ARCHIVES OF PHARMACAL RESEARCH, v.35, no.7, pp.1279 - 1286
Abstract
Alzheimer's disease (AD) is the most prevalent cause of dementia in the elderly people. The disease is pathologically characterized by extracellular deposition of beta-amyloid peptide (A beta), cholinergic neurodegeneration and elevation of acetylcholine esterase (AChE) activity in the affected regions. In this study, we investigated the effects of obovatol on memory dysfunction, which was caused by scopolamine. Obovatol (0.2, 0.5 and 1 mg/kg for 7 day) attenuated scopolamine (1 mg/kg, i.p.)-induced amnesia in a dose-dependent manner, as revealed by the Morris water maze test and step-through passive avoidance test. Mechanism studies exhibited that obovatol dose-dependently alleviated scopolamine-induced increase in A beta generation and beta-secretase activity in the cortex and hippocampus. Obovatol also attenuated scopolamine-induced rise in AChE activity in the cortex and hippocampus. Obovatol might rescue scopolamine-mediated impaired learning and memory function by attenuating A beta accumulation and stabilizing cholinergic neurotransmission, which suggests that the natural compound could be a useful agent for the prevention of the development or progression of AD neurodegeneration.
URI
http://hdl.handle.net/YU.REPOSITORY/27623http://dx.doi.org/10.1007/s12272-012-0719-1
ISSN
0253-6269
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약학대학 > 약학부 > Articles
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