Evidence map›Paper›PMID 41687921›Full record

ArticleBiomedical journal2026

GR/HDAC2/synaptic complexes in hippocampal CA1 mediate the antidepressant effects of magnolol.

Yu-Qian Jiang, Qing-Yu Kuang, Yuan Xu, Yi-Xiang Xu, Jie Cheng, Li-Tao Yi

Abstract read
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In one paragraph

Article in Biomedical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Yu-Qian JiangDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China; Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Qing-Yu KuangDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China.
Yuan XuDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China.
Yi-Xiang XuDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China.
Jie ChengDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China.
Li-Tao YiDepartment of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, Fujian, China; Institute of Pharmaceutical Engineering, Huaqiao University, Xiamen, Fujian, China; Fujian Provincial Key Laboratory of Biochemical Technology, Huaqiao University, Xiamen, Fujian, China. Electronic address: litaoyi@hqu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDepression is a multifactorial neuropsychiatric disorder linked to neuroinflammation and epigenetic dysregulation, particularly in histone acetylation. Although magnolol has demonstrated antidepressant-like properties, its precise molecular mechanisms remain unclear. This study aimed to evaluate the antidepressant effects of magnolol and its influence on epigenetic regulation of synaptic plasticity in a chronic unpredictable mild stress (CUMS) mouse model. MATERIAL AND

methodsC57BL/6 mice subjected to CUMS were treated orally with magnolol. Depressive-like behaviors were assessed using standard behavioral tests. Expression levels of histone deacetylase 2 (HDAC2), synaptic proteins such as neuroligin-1 (NLGN1) and neurexin-1β (NRXN1β), and their associated co-localized puncta were examined. Golgi staining and immunofluorescence were performed to assess dendritic spine density and DCX-positive cell population in the hippocampus.

resultsMagnolol treatment alleviated depressive-like behaviors, evidenced by increased sucrose preference and reduced immobility in behavioral assays. It also attenuated hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, as shown by normalization of serum corticosterone levels and restoration of glucocorticoid receptor (GR) expression in the hippocampal CA1 region. At the molecular level, magnolol reduces HDAC2 expression, which may be associated with altered histone acetylation, thus upregulation of NLGN1 and NRXN1β, enhancing the formation of pre- and postsynaptic co-localized puncta. Additionally, magnolol promoted hippocampal DCX-positive cell population and synaptogenesis, supporting improvements in structural and functional neuroplasticity.

conclusionOur findings demonstrate the ability of magnolol to modulate histone acetylation and synaptic architecture involved in its antidepressant-like action. These results provide a foundation for further exploration of magnolol-based interventions targeting epigenetic and synaptic mechanisms in depression.

Indexed as

Antidepressive AgentsBiphenyl CompoundsCA1 Region, HippocampalDepressionHistone Deacetylase 2LignansReceptors, GlucocorticoidSynapsesAnimalsDoublecortin ProteinMaleMiceMice, Inbred C57BLAntidepressive AgentsBiphenyl CompoundsDcx protein, mouseDoublecortin ProteinHdac2 protein, mouseHistone Deacetylase 2LignansmagnololReceptors, GlucocorticoidDepressionGlucocorticoid receptor (GR)Histone deacetylase 2 (HDAC2)MagnololSynaptogenesis

Identifiers

PMID41687921
PMCPMC13226807

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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.