Abstract
This study measured amyloid-beta (Aβ), interleukin-1 beta (IL-1β), and glial fibrillary acidic protein (GFAP) expression in the hippocampus of Alzheimer's disease (AD) rat models to elucidate the mechanism of anti-inflammatory effect of ginsenoside Rb1 in AD. Eighty-four male Wistar rats were randomly divided into seven groups, learning and memory impairment was induced by Ap1-40 to establish AD rat model. Learning and memory abilities were assessed by a Morris water maze experiment. Immunohistochemistry, RT-PCR and Western blotting were used to measure IL-1β, Aβ and GFAP expression. Nissl staining and methenamine silver staining were performed to observe the morphology of neurons and Nissl Body, and to detect amyloid protein particle deposition. ELISA and LC-MS/MS were applied to detect Aβ1-42 and byproducts of S/MS were applied to IAT, VIV, ITL, VVIA, TVI, and VIT). Ginsenoside Rb1 administration could relieve cognitive deficit, and decrease expressions of IL-1β, Aβ, and GFAP. Neurons and Nissl Body were improved and plaques deposition was decreased obviously after treatment of ginsenoside Rb1, especially in medium dose of ginsenoside Rb1. Ginsenoside Rb1 can increase productions of Aβ1-42 and byproducts of β- and γ-secretase. Collected evidence supported that ginsenoside Rb1 improves learning and memory in AD rat by altering the amyloidogenic process of APP into non-amyloidogenic process, to exert its anti-inflammatory function.
Full text
