|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|2592298||1131971||2016||6 صفحه PDF||سفارش دهید||دانلود کنید|
• Cognition-enhancing effects of Cereboot™, an American ginseng extract, were investigated.
• Cereboot™ inhibited Aβ cytotoxicity and enhanced ChAT expression in F3.ChAT cells.
• Cereboot™ recovered cognitive function of Aβ1-42-challenged mice.
• Neuronal integrity and acetylcholine level were restored by treatment with Cereboot™.
In Alzheimer disease (AD), amyloid-beta (Aβ) peptides induce the degeneration of presynaptic cholinergic system, in which decreased activity of enzyme choline acetyltransferase (ChAT) responsible for acetylcholine synthesis is observed. Cereboost™, an extract of American ginseng extract, contains a high concentration of Rb1 ginsenoside which is a well-known ingredient improving human cognitive function. We investigated the effects of Cereboost™ on learning and memory function of mice challenged with an Aβ1-42 peptide and the underlying mechanisms in vitro. Cereboost™ protected against Aβ1-42-induced cytotoxicity in F3.ChAT stem cells, and enhanced the ChAT gene expression. Aβ1-42 injection into the mouse brain impaired the cognitive function, which was recovered by oral administration of Cereboost™. In addition, Cereboost™ restored brain microtubule-associated protein 2 and synaptophysin as well as acetylcholine concentration. The results demonstrate that Cereboost™ administration recovered the cognitive function of AD model animals by enhancing acetylcholine level via ChAT gene expression and neuroprotection.
Journal: Regulatory Toxicology and Pharmacology - Volume 78, July 2016, Pages 53–58