文献类型：期刊文献

英文题名：Optimal Formula of Angelica sinensis Ameliorates Memory Deficits in β-amyloid Protein-induced Alzheimer's Disease Rat Model

作者：Wang, Hu-Ping[1];Wu, Hong-Yan[1];Ma, Chun-Lin[1];Zeng, Qing-Tao[1];Zhu, Kai-Min[1];Cui, Shu-Mei[1];Li, Hai-Long[2];Wu, Guo-Tai[3];Wu, Zhi-Wei[1];He, Jian-Zheng[1]

第一作者：王虎平

通信作者：Wang, HP[1]

机构：[1]Gansu Univ Chinese Med, Basic Med Coll, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Clin Med Coll, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Pharm Coll, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学基础医学院（敦煌医学研究所）

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Basic Med Coll, Lanzhou 730000, Peoples R China.|[107351d2d02a88e1f325f]甘肃中医药大学基础医学院（敦煌医学研究所）;[10735]甘肃中医药大学;

年份：2022

卷号：42

期号：1

起止页码：39

外文期刊名：CURRENT MEDICAL SCIENCE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000751571000001)】；

基金：This project was supported by the National Natural Science Foundation of China (No. 81960828).'

语种：英文

外文关键词：optimal formula of Angelica sinensis; Alzheimer's disease; amyloid beta aggregation; oxidative stress; neuroinflammation

摘要：Objective: Angelica (A.) sinensis is used as a traditional medical herb for the treatment of neurodegeneration, aging, and inflammation in Asia. A. sinensis optimal formula (AOF) is the best combination in A. sinensis that has been screened to rescue the cognitive ability in -amyloid peptide (A beta(25-35))-treated Alzheimer's disease (AD) rats. The objective of this study was to investigate the effect of AOF on the learning and memory of AD rats as well as to explore the underlying mechanisms. Methods: Male Wistar rats were infused with A beta(25-35) for AD model induction or saline (negative control). Five groups of AD rats were fed on AOF at 20, 40, or 80 mL/kg every day, donepezil at 0.9 mg/kg every day (positive control), or an equal volume of water (AD model) intragastrically once a day for 4 weeks, while the negative control rats were fed on water. The Morris water maze test was used to evaluate the cognitive function of the rats. The A beta accumulation, cholinergic levels, and antioxidative ability were detected by ELISA. Additionally, the candidate mechanism was determined by gene sequencing and quantitative real-time polymerase chain reaction. Results: The results showed that AOF administration significantly ameliorated A beta(25-35)-induced memory impairment. AOF decreased the levels of amyloid-beta precursor protein and A beta in the hippocampus, rescued the cholinergic levels, increased the activity of superoxide dismutase, and decreased the malondialdehyde level. In addition, AOF inhibited the expression of IL1b, Mpo, and Prkcg in the hippocampus. Conclusion: These experimental findings illustrate that AOF prevents the decrease in cognitive function and A beta deposits in A beta(25-35)-treated rats via modulating neuroinflammation and oxidative stress, thus highlighting a potential therapeutic avenue to promote the co-administration of formulas that act on different nodes to maximize beneficial effects and minimize negative side effects.