Evidence map›Paper›PMID 35303280›Full record

ArticleMolecular neurobiology2022

Kai-Xin-San Inhibits Tau Pathology and Neuronal Apoptosis in Aged SAMP8 Mice.

Ya-Nan Jiao, Jing-Sheng Zhang, Wen-Jun Qiao, Shu-Yu Tian, Yi-Bin Wang, Chun-Yan Wang, Yan-Hui Zhang, Qi Zhang, Wen Li, Dong-Yu Min and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 3 pooled it
4.5field-weighted citation impact, top 4% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Efficacy and possible mechanism ofFrontiers in pharmacology · 2026
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  3. Frontiers in pharmacology · 2023
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  15. Identification ofInternational journal of molecular sciences · 2023
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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

11 authors at 3 institutions in 1 country.

Ya-Nan JiaoHealth Sciences Institute, China Medical University, Shenyang, China.
Jing-Sheng ZhangAffiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Wen-Jun QiaoAffiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Shu-Yu TianHealth Sciences Institute, China Medical University, Shenyang, China.
Yi-Bin WangHealth Sciences Institute, China Medical University, Shenyang, China.
Chun-Yan WangHealth Sciences Institute, China Medical University, Shenyang, China.
Yan-Hui ZhangSchool of Fundamental Sciences, China Medical University, Shenyang, China.
Qi ZhangHealth Sciences Institute, China Medical University, Shenyang, China.
Wen LiHealth Sciences Institute, China Medical University, Shenyang, China.
Dong-Yu MinAffiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, China. yangyongju@lnutcm.edu.cn.
Zhan-You WangHealth Sciences Institute, China Medical University, Shenyang, China. Wangzy@cmu.edu.cn.ORCID http://orcid.org/0000-0003-0807-9916
China Medical University · CNAffiliated Hospital of Liaoning University of Traditional Chinese Medicine · CNLiaoning University of Traditional Chinese Medicine · CN

Funding

Department of Science and Technology of Liaoning Province No.2019JH2/10300003
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related neurological disorder. Currently, there is no effective cure for AD due to its complexity in pathogenesis. In light of the complex pathogenesis of AD, the traditional Chinese medicine (TCM) formula Kai-Xin-San (KXS), which was used for amnesia treatment, has been proved to improve cognitive function in AD animal models. However, the active ingredients and the mechanism of KXS have not yet been clearly elucidated. In this study, network pharmacology analysis predicts that KXS yields 168 candidate compounds acting on 863 potential targets, 30 of which are associated with AD. Enrichment analysis revealed that the therapeutic mechanisms of KXS for AD are associated with the inhibition of Tau protein hyperphosphorylation, inflammation, and apoptosis. Therefore, we chose 7-month-old senescence-accelerated mouse prone 8 (SAMP8) mice as AD mouse model, which harbors the behavioral and pathological hallmarks of AD. Subsequently, the potential underlying action mechanisms of KXS on AD predicted by the network pharmacology analyses were experimentally validated in SAMP8 mice after intragastric administration of KXS for 3 months. We observed that KXS upregulated AKT phosphorylation, suppressed GSK3β and CDK5 activation, and inhibited the TLR4/MyD88/NF-κB signaling pathway to attenuate Tau hyperphosphorylation and neuroinflammation, thus suppressing neuronal apoptosis and improving the cognitive impairment of aged SAMP8 mice. Taken together, our findings reveal a multi-component and multi-target therapeutic mechanism of KXS for attenuating the progression of AD, contributing to the future development of TCM modernization, including KXS, and broader clinical application.

Indexed as

Alzheimer DiseaseDrugs, Chinese HerbalAnimalsApoptosisDisease Models, AnimalMedicine, Chinese TraditionalMicetau ProteinsDrugs, Chinese HerbalKai-Xin-Santau ProteinsApoptosisInflammationKai-Xin-SanNetwork pharmacologyTau hyperphosphorylation

Identifiers

PMID35303280
PMCPMC9016055
OpenAlexW4220846033

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.