PMID- 38081400
OWN - NLM
STAT- MEDLINE
DCOM- 20240101
LR  - 20240106
IS  - 1872-7573 (Electronic)
IS  - 0378-8741 (Linking)
VI  - 321
DP  - 2024 Mar 1
TI  - Polysaccharide from Polygala tenuifolia alleviates cognitive decline in 
      Alzheimer's disease mice by alleviating Abeta damage and targeting the ERK pathway.
PG  - 117564
LID - S0378-8741(23)01434-4 [pii]
LID - 10.1016/j.jep.2023.117564 [doi]
AB  - ETHNOPHARMACOLOGICAL RELEVANCE: Polygala tenuifolia is used in a variety of 
      Chinese medicine prescriptions for the classic dementia treatment, and 
      polysaccharide is an important active component in the herb. AIM OF THE STUDY: 
      This study investigated the in vivo anti-Alzheimer's disease (AD) activity of the 
      polysaccharide PTPS from Polygala tenuifolia using the senescence-accelerated 
      mouse/prone8 (SAMP8) model and explored its molecular mechanism to lay the 
      foundation for the development of polysaccharide-based anti-AD drugs. MATERIALS 
      AND METHODS: The Morris water maze test (MWM)was used to detect changes in the 
      spatial cognitive ability of mice, and Nissl staining was applied to observe the 
      state of neurons in the classic hippocampus. The levels of acetylcholine (ACh) 
      and acetylcholinesterase (AChE) were measured by ELISA. Immunofluorescence was 
      used to reflect beta-amyloid (Abeta) levels in brain tissue. Apoptosis was evaluated by 
      TdT-mediated dUTP Nick-End Labeling (TUNEL) method. The status of dendritic 
      branches and spines was observed by Golgi staining. Meanwhile, the expression 
      levels of recombinant human insulin-degrading enzyme (IDE), brain-derived 
      neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), extracellular 
      regulated protein kinases (ERK), and cAMP-response element binding protein (CREB) 
      proteins were determined by Western blotting. RESULTS: PTPS improves spatial 
      cognitive deficits in AD mice, reduces cellular damage in the CA3 region of the 
      hippocampus, maintains the balance of the cholinergic system, and exerts an 
      anti-AD effect in vivo. The molecular mechanism of its action may be related to 
      the reduction of Abeta deposition as well as the activation of ERK pathway-related 
      proteins with enhanced synaptic plasticity. CONCLUSIONS: PTPS is able to exert 
      anti-AD activity in vivo by mitigating Abeta damage and targeting the ERK pathway.
CI  - Copyright (c) 2023 Elsevier B.V. All rights reserved.
FAU - Li, Yuanyuan
AU  - Li Y
AD  - School of Pharmaceutical Sciences, Shandong University of Traditional Chinese 
      Medicine, Key Laboratory of Medicinal Fungi and Resource Development in Shandong 
      Province, Jinan 250355, China.
FAU - Wu, Haoran
AU  - Wu H
AD  - School of Medicine, Southern University of Science and Technology, Shenzhen 
      518055, China.
FAU - Liu, Maoxuan
AU  - Liu M
AD  - Center for Protein and Cell-Based Drugs, Institute of Biomedicine and 
      Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of 
      Sciences, Shenzhen 518055, China.
FAU - Zhang, Zhiyuan
AU  - Zhang Z
AD  - School of Pharmaceutical Sciences, Shandong University of Traditional Chinese 
      Medicine, Key Laboratory of Medicinal Fungi and Resource Development in Shandong 
      Province, Jinan 250355, China.
FAU - Ji, Yuning
AU  - Ji Y
AD  - School of Foreign Languages, Shandong University of Traditional Chinese Medicine, 
      Jina, China.
FAU - Xu, Lingchuan
AU  - Xu L
AD  - School of Pharmaceutical Sciences, Shandong University of Traditional Chinese 
      Medicine, Key Laboratory of Medicinal Fungi and Resource Development in Shandong 
      Province, Jinan 250355, China.
FAU - Liu, Yuhong
AU  - Liu Y
AD  - School of Pharmaceutical Sciences, Shandong University of Traditional Chinese 
      Medicine, Key Laboratory of Medicinal Fungi and Resource Development in Shandong 
      Province, Jinan 250355, China. Electronic address: yhliu@sdutcm.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20231209
PL  - Ireland
TA  - J Ethnopharmacol
JT  - Journal of ethnopharmacology
JID - 7903310
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 3.1.1.7 (Acetylcholinesterase)
RN  - 0 (Amyloid beta-Peptides)
SB  - IM
MH  - Mice
MH  - Humans
MH  - Animals
MH  - *Alzheimer Disease/drug therapy/metabolism
MH  - *Polygala/chemistry
MH  - Protein Kinases/metabolism
MH  - MAP Kinase Signaling System
MH  - Acetylcholinesterase/metabolism
MH  - Hippocampus
MH  - Amyloid beta-Peptides/metabolism
MH  - *Cognitive Dysfunction/drug therapy/metabolism
MH  - Disease Models, Animal
OTO - NOTNLM
OT  - Activity mechanism
OT  - Alzheimer's disease
OT  - Polygala tenuifolia polysaccharide
COIS- Declaration of Competing interest I would like to declare on behalf of my 
      co-authors that the work has not been published previously, and not under 
      consideration for publication elsewhere, in whole or in part. No conflict of 
      interest exits in the submission of this manuscript and the manuscript is 
      approved by all authors for publication.
EDAT- 2023/12/12 00:42
MHDA- 2024/01/02 11:46
CRDT- 2023/12/11 19:23
PHST- 2023/10/05 00:00 [received]
PHST- 2023/11/13 00:00 [revised]
PHST- 2023/12/05 00:00 [accepted]
PHST- 2024/01/02 11:46 [medline]
PHST- 2023/12/12 00:42 [pubmed]
PHST- 2023/12/11 19:23 [entrez]
AID - S0378-8741(23)01434-4 [pii]
AID - 10.1016/j.jep.2023.117564 [doi]
PST - ppublish
SO  - J Ethnopharmacol. 2024 Mar 1;321:117564. doi: 10.1016/j.jep.2023.117564. Epub 
      2023 Dec 9.