Evidence map›Paper›PMID 34705126›Full record

ArticleJournal of natural medicines2022

Magnolol upregulates CHRM1 to attenuate Amyloid-β-triggered neuronal injury through regulating the cAMP/PKA/CREB pathway.

Gemin Zhu, Yuan Fang, Xiaoli Cui, Ruihua Jia, Xiaogang Kang, Rui Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of natural medicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Magnolol acts as a neurorestorative agent in an AExperimental and therapeutic medicine · 2025
    Article
  6. Heliyon · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
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 at 4 institutions in 1 country.

Gemin Zhu *Department of Neurology, Xi'an Central Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, 710003, People's Republic of China.
Yuan Fang *Department of Neurosurgery, Xi'an No. 3 Hospital, The Affiliated Hospital of Northwest University, Xi'an, 710018, People's Republic of China.
Xiaoli CuiDepartment of Neurology, Shaanxi Provincial People's Hospital, No. 256 West Friendship Road, Xi'an, 710068, People's Republic of China.
Ruihua JiaDepartment of Neurology, Shaanxi Provincial People's Hospital, No. 256 West Friendship Road, Xi'an, 710068, People's Republic of China.
Xiaogang KangDepartment of Neurology, Xijing Hospital, Air Force Medical University, No. 15 Changle West Road, Xi'an, 710032, People's Republic of China. paraq@163.com.
Rui ZhaoDepartment of Neurology, Shaanxi Provincial People's Hospital, No. 256 West Friendship Road, Xi'an, 710068, People's Republic of China. ruizhao3845@126.com.
Shaanxi Provincial People's Hospital · CNNorthwest University · CNXi'an Jiaotong University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disease characterized by neuronal degeneration and hyperphosphorylated Tau. Magnolol is an active component isolated from Magnolia officinalis with potential neuroprotection activity. However, the function and mechanism of magnolol in AD progression is largely uncertain. In present study, the biomarkers related to AD and magnolol were predicted by bioinformatics analyses. The key biomarker levels were predicted by GSE5281 and GSE36980 using AlzData. Cell viability was detected by CCK-8 assay. mRNA and protein levels were examined by qRT-PCR and western blotting assays. Cell apoptosis was investigated by caspase-3 activity and flow cytometry analyses. The cAMP/PKA/CREB signaling was evaluated by ELISA and western blotting analyses. The results showed that CHRM1 was a key biomarker for magnolol against AD progression. Magnolol attenuated Aβ-induced viability inhibition, Tau hyperphosphorylation and apoptosis in SH-SY5Y cells by upregulating CHRM1. In addition, the cAMP signaling might be a potential pathway of CHRM1 in AD. Magnolol contributed to activation of the cAMP/PKA/CREB pathway through enhancing CHRM1 level. Inactivation of the cAMP/PKA/CREB signaling reversed the suppressive effect of magnolol on Tau hyperphosphorylation and apoptosis in Aβ-treated SH-SY5Y cells. As a conclusion, magnolol mitigated Aβ-induced Tau hyperphosphorylation and neuron apoptosis by upregulating CHRM1 and activating the cAMP/PKA/CREB pathway.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesApoptosisBiphenyl CompoundsHumansLignansNeuronsReceptor, Muscarinic M1Amyloid beta-PeptidesBiphenyl CompoundsCHRM1 protein, humanLignansmagnololReceptor, Muscarinic M1Alzheimer’s diseaseAmyloid-βApoptosiscAMP/PKA/CREB pathwayCHRM1MagnololTau hyperphosphorylation

Identifiers

PMID34705126
OpenAlexW3209798418

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.