摘要： Background：Beta-amyloid （Aβ） deposition，associated neuronal apoptosis and neuroinflammation are considered as important factors leading to cognitive deficits in Alzheimer’s disease（ AD）. Icariside Ⅱ（ ICS Ⅱ），an active fl avonoid compound derived from Epimedium brevicornum Maxim，has been extensively used to treat erectile dysfunction，osteoporosis and dementia. Recently，ICS Ⅱ attracts great interest due to its broad-spectrum anti-cancer property. ICS Ⅱ shows an antiinflammatory potential both in cancer treatment and cerebral ischemia-reperfusion. It is not yet clear whether the anti-inflammatory effect of ICS Ⅱ could delay progression of AD. Therefore，the current study aimed to investigate the effects of ICS Ⅱ on the behavioral deficits，Aβ levels，neuroinfl ammatory responses and apoptosis in Aβ25-35 treated rats. Methods：Rats subjected to bilateral hippocampal injection of Aβ25-35 or normal saline were administered with ICS Ⅱ 20 mg·kg-1 or vehicle once a day for consecutive 15 days. Learning and memory function was evaluated using Morris water maze. The neuronal morphology in hippocampus was examined by HE staining and Nissl staining，respectively. Neuronal apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assay. The activation of microglia and astrocytes were analyzed by immunohistochemistry. The expression of interleukin-1β（ IL-1β），cyclooxygenase-2（COX-2），tumor necrosis factor-α（ TNF-α） and inducible nitric oxide synthase（ iNOS） were detected by quantitative real-time polymerase chain reaction（ qRT-PCR） and Western blot. The expression of caspase-3，Bax and Bcl-2 and the content of beta-amyloid were measured by Western blot. Results：Rats treated with Aβ25-35 displayed cognitive impairment，neuronal damage，along with the increase of Aβ，infl ammation and apoptosis in the hippocampus. However，treatment with ICS Ⅱ 20 mg·kg-1 could improve the cognitive defi cits，ameliorate neuronal death，and reduce the levels of Aβ in the hippocampus. Furthermore，ICS Ⅱ could suppress microglial and astrocytic activation，inhibit expression of IL-1b，TNF-a，COX-2，and iNOS mRNA and protein，and attenuate the Aβ induced Bax/Bcl-2 ratio elevation and caspase-3 activation. Conclusions：These fi ndingssuggest that ICS Ⅱ couldreverse Aβ-induced cognitive deficits，possibly via the inhibition of neuroinfl ammation and apoptosis，which suggested a potential protective effect of ICS Ⅱ on AD.