文献类型：期刊文献

英文题名：3,6′-Disinapoyl sucrose alleviates cognitive deficits in APP/PS1 transgenic mice

作者：Yuan, Jiaqi[1];He, Mengjie[1];Dai, Xueling[1];Huo, Qing[1];Chang, Ping[1];Zhang, Jing[1];Wang, Shuo[2];Sun, Yaxuan[1]

第一作者：Yuan, Jiaqi

通讯作者：Sun, YX[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing, Peoples R China;[2]Nankai Univ, Sch Med, Tianjin Key Lab Food Sci & Hlth, Tianjin, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, 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;[114172]北京联合大学应用文理学院;

年份：2023

卷号：130

期号：5

起止页码：1174-1182

外文期刊名：JOURNAL OF NEUROPHYSIOLOGY

收录：;Scopus(收录号：2-s2.0-85175585697);WOS:【SCI-EXPANDED(收录号:WOS:001112749700001)】；

基金：This work was supported by the Academic Research Projects of Beijing Union University (No. ZK80202102) and the National Natural Science Foundation of China (11975048).

语种：英文

外文关键词：Alzheimer's disease; apoptosis; CREB/BDNF signal pathway; 3,6'-disinapoyl sucrose; Morris water maze

摘要：Alzheimer's disease (AD) is a neurodegenerative disorder with insidious onset and progressive development. There is an urgent need to find drugs that prevent and slow AD progression. We focus our attention on 3,6 '-disinapoyl sucrose (DISS), an oligosaccharide with antidepressant and antioxidant activities. In this work, APP/PS1 transgenic mice were used to explore the neuroprotective impact of DISS to provide new applications for prevention and therapy of AD. This study aims to assess DISS's neuroprotective impact on learning and memory deficits in APP/PS1 transgenic mice using behavioral tests (Morris water maze, novel object recognition test, and passive avoidance test). Morphological alterations of hippocampus neurons were observed by Nissl staining and neuronal apoptosis was assessed by TUNEL assay. By using ELISA, the expressions of inflammatory factors were evaluated, and Western blotting was used to measure the protein expressions of neuron-related regulators in the hippocampus. DISS significantly ameliorated the cognitive disorder in APP/PS1 transgenic mice, reduced apoptosis by decreasing the ratio of Bax/B-cell lymphoma/leukemia-2 (Bcl-2) in hippocampal neurons, and restored the abnormal secretion of inflammatory factors (IL-2, TNF-alpha, IL-1 beta, and IL-6). Moreover, the gavage of high-dose DISS can boost the expressions of CREB/brain-derived neurotrophic factor (BDNF). Overall, our results indicate that DISS improves cognitive function in APP/PS1 transgenic mice by inhibiting neural apoptosis and activating the CREB/BDNF signal pathway.