文献类型：期刊文献

英文题名：Protective effects of fisetin in an A beta(1-42)-induced rat model of Alzheimer's disease

作者：Wang, Yunting[1];Wu, Xueling[1];Ren, Wujiang[1];Liu, Yanxia[1];Dai, Xueling[1];Wang, Shuo[2];Huo, Qing[1];Sun, Yaxuan[1]

第一作者：Wang, Yunting

通讯作者：Wang, YT[1]

机构：[1]Beijing Union Univ, Dept Food Sci & Engn, Coll Biochem Engn, Beijing, Peoples R China;[2]Nankai Univ, Coll Environm Sci & Engn, Tianjin, Peoples R China

第一机构：北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Dept Food Sci & Engn, Coll Biochem Engn, Beijing, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;

年份：2023

卷号：61

期号：2

起止页码：196-208

外文期刊名：FOLIA NEUROPATHOLOGICA

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001033454500010)】；

基金：& nbsp;This work was supported by the National Natural Science Foundation of China [grant number 11975048] ; Beijing Union University Open Project [grant number SWHX202103] and Beijing Union University scientific research project funding [grant number XP202007] .

语种：英文

外文关键词：Alzheimer's disease; A beta(1-42); fisetin; protective effects; mechanism

摘要：Alzheimer's disease (AD) is a chronic, neurodegenerative disorder that affects the central nervous system and is found predominantly in elderly populations. As amyloid beta protein (A beta) is one of the key players responsible for the pathogenesis of AD, we sought to investigate the protective effects of fisetin in an Ab 1-42-induced rat model of AD. In this model, the protective effects of fisetin on learning and memory impairment induced by A beta(1-42) were determined via the Morris water maze and passive avoidance test. Furthermore, the antioxidant activity, anti-inflammation, and apoptosis effect of fisetin were investigated using biochemical and immunohistochemical methods. The results showed that intragastric (i.g.) administration of fisetin (100, 50, and 25 mg/kg) improved previous learning and memory impairments in A beta(1-42)-treated rats. Hippocampal tissue from these fisetin-treated rats revealed that the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) were markedly enhanced, and that the levels of malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were significantly reduced. Meanwhile, fisetin also significantly attenuated A beta(1-42)-induced cholinergic dysfunction such as elevated the activity of choline acetyltransferase (ChAT) and reduced the activity of acetylcholine esterase (AChE). In addition, hippocampal tissue obtained from fisetin-treated rats revealed a reversal of A beta(1-42)-induced effects on apoptotic pathway protein (caspase-3) expression and inflammatory response of glial fibrillary acidic protein (GFAP). This indicated that the amount of degenerating hippocampal neurons with apoptotic features was dramatically reduced after treatment with fisetin. Collectively, these findings suggest that fisetin has potential as a treatment agent for Alzheimer's disease and that its effects occur through several mechanisms, including inhibition of oxidative stress, adjustments to previous cholinergic dysfunction, anti-inflammatory actions, and decreased apoptotic activity.