Evidence map›Paper›PMID 40879814›Full record

ArticleMetabolic brain disease2025

Neuroprotective effects of Yangming-Kaixin-Yizhi formula in Alzheimer's disease: dual regulation of PI3K/Akt and p38 MAPK signaling via network pharmacology and experimental approaches.

Jing Lei, Jiaming Li, Wei Wu, Rui Xiong, Yao Liu, Yong Tang

Abstract read
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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Jing Lei *Department of Pharmacy, Daping Hospital, Army Medical University, Chongqing, China.ORCID 0009-0002-5864-6333
Jiaming Li *Department of Pharmacy, Daping Hospital, Army Medical University, Chongqing, China.
Wei Wu *Department of Pharmacy, Daping Hospital, Army Medical University, Chongqing, China.
Rui XiongDepartment of Pharmacy, Jiangbei Campus of The First Affiliated Hospital of Army Medical University (The 958th Hospital of Chinese People's Liberation Army), Chongqing, China. xiongrui@tmmu.edu.cn.ORCID 0000-0001-5008-0094
Yao LiuDepartment of Pharmacy, Daping Hospital, Army Medical University, Chongqing, China. liuyao@tmmu.edu.cn.ORCID 0000-0001-7507-2410
Yong TangLaboratory Animal Centre, Model Animal and Human Disease Research of Luzhou Key Laboratory, Southwest Medical University, Luzhou, China. tangy1989@yeah.net.ORCID 0000-0002-3686-8990

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a neurodegenerative disease characterized by progressive cognitive decline, the pathogenesis of Alzheimer's disease (AD) is still poorly understood, and there is no effective cure currently available. Traditional Chinese medicine (TCM) prescription Yangming-Kaixin-Yizhi formula (YKY) has been clinically applied for the treatment of memory loss related disorders for more than 300 years with remarkable efficacy, but its pharmacological mechanism remains unclear. This study aimed to investigate the therapeutic effects of YKY on AD and its molecular mechanisms. We evaluated YKY's ameliorative effects on the AD phenotype in 3xTg-AD mice using the Morris water maze, histopathological staining, and immunofluorescence assays. The major chemical components of YKY were identified by UPLC-QTOF-MS/MS. Network pharmacology was employed to analyze the molecular mechanisms of YKY in treating AD, followed by validation of its regulatory effects on key pathways through immunofluorescence experiments and molecular docking. The results showed that YKY could significantly improve learning and memory ability, neuronal loss, β-amyloid deposition and glial cell activation in 3xTg-AD mice. 48 chemical components were identified from YKY, and network pharmacology analysis of them showed that YKY may improve AD by regulating apoptosis, PI3K/Akt and MAPK pathways. Immunofluorescence and molecular docking results also confirmed the regulatory effect of YKY on key targets of apoptosis, PI3K/Akt and p38 MAPK pathways. In conclusion, by integrating animal experiments and network pharmacology, the present study revealed the mechanism of YKY in inhibiting neuronal apoptosis by regulating PI3K/Akt and p38 MAPK pathways, which providing modern scientific evidence for the traditional clinical application of YKY.

Indexed as

Alzheimer DiseaseDrugs, Chinese HerbalMAP Kinase Signaling SystemNeuroprotective Agentsp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktAnimalsDisease Models, AnimalMaleMiceMice, TransgenicMolecular Docking SimulationNetwork PharmacologyPhosphatidylinositol 3-KinasesSignal TransductionDrugs, Chinese HerbalNeuroprotective Agentsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt3xTg-AD miceAlzheimer’s diseaseNetwork pharmacologyp38 MAPKPI3K/AktYangming-Kaixin-Yizhi formula

Identifiers

PMID40879814

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.