Evidence map›Paper›PMID 40355775›Full record

ArticleCell biochemistry and biophysics2025

The Paeonol of Total Glucosides of White Peony Regulates the Differentiation of CD4+Treg Cells through the EP300/Foxp3 Axis to Relieve Pulmonary Fibrosis in Mice.

Muyun Yan, Qing Wang, Hongzhong Yang, Da Liu, Weijun Liang, Huamei Chen

Abstract read
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In one paragraph

Article in Cell biochemistry and biophysics, 2025. 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

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

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.

Muyun YanDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.
Qing WangDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.
Hongzhong YangDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.
Da LiuDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China. 2018050679@usc.edu.cn.
Weijun LiangDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.
Huamei ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.

Funding

Natural Science Foundation of Changsha kq2202047Natural Science Foundation of Changsha kq2202053
6 · The paper itself

Abstract

Pulmonary fibrosis is a chronic progressive lung disease that can lead to lung structural damage and respiratory failure. This study aimed to investigate whether paeonol could improve pulmonary fibrosis in mice by regulating through the EP300/Foxp3 axis. We established a mouse model of pulmonary fibrosis. Total glucosides of white peony (TGP) were used to treat the animal model, and lung injury was observed using HE and Masson staining. Inflammatory factor levels in bronchoalveolar lavage fluid were detected using ELISA. Network pharmacology analysis was conducted to explore the components, shared targets, and signaling pathways of pulmonary fibrosis and TGP. Molecular docking was performed to observe the binding of paeonol, a component of TGP, to the target EP300. CD4+T cells were collected and co-cultured with MPPF cells, followed by intervention with TGP and paeonol. The ratio of CD4+T/Treg cells was measured in vitro, and immunofluorescence was used to detect the intensity of α-SMA. Network pharmacology revealed that one of the key components of TGP is paeonol, and the signaling pathway associated with pulmonary fibrosis is the Foxp3 signaling pathway. TGP effectively inhibited the secretion of lung inflammatory factors TGF-β1, IFN-γ, IL-2, and IL-17 in mic. Paeonol, an effective component of TGP, could bind to EP300 at the molecular level. Both TGP and paeonol inhibited the expression of EP300 in CD4+T and MPPF cells, enhanced the proportion of Treg cells in CD4+T, and reduced the expression of Collagen I and α-SMA in MPPF cells. TGP can effectively inhibit lung inflammation and fibrosis progression in mice. Paeonol regulating CD4+Treg cell differentiation through the EP300/Foxp3 axis. This study may provide new insights into how TGP improves pulmonary fibrosis in mice.

Indexed as

AcetophenonesCell DifferentiationForkhead Transcription FactorsGlucosidesPaeoniaPulmonary FibrosisT-Lymphocytes, RegulatoryAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMolecular Docking SimulationSignal TransductionAcetophenonesForkhead Transcription FactorsFoxp3 protein, mouseGlucosidespaeonolCD4+TregEP300Foxp3PaeonolTotal glucosides of white peony

Identifiers

PMID40355775

What OpenQuestion holds

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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.