Evidence map›Paper›PMID 41937438›Full record

ArticleImmunity, inflammation and disease2026

Polydatin Relieves Airway Remodeling by Inhibiting P2X7R-NLRP3-Mediated Excessive Autophagy in Asthma.

Guangxing Li, Liangchang Li, Zhiguang Wang, Yihua Piao, Yilan Song, Li Li, Chang Xu, Xiaowan Li, Guanghai Yan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, inflammation and disease, 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

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

9 authors.

Guangxing LiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Liangchang LiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Zhiguang WangJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Yihua PiaoJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Yilan SongJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.ORCID https://orcid.org/0000-0001-6428-5947
Li LiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Chang XuJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Xiaowan LiJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.
Guanghai YanJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, Jilin, China.ORCID https://orcid.org/0000-0001-8058-7822

Funding

Jilin Province Science and Technology Department project 20240404025ZPNational Natural Science Foundation of China 32560211
6 · The paper itself

Abstract

backgroundAsthma is characterized by chronic airway inflammation and remodeling. Polydatin (PD), a natural compound, has shown anti-inflammatory potential, but its role in asthma-related airway remodeling and the underlying mechanisms involving the P2X7R-NLRP3 inflammasome axis and autophagy remain unclear.

methodsAn ovalbumin-induced asthmatic mouse model and primary airway smooth muscle cells (ASMCs) were used. Mice were treated with PD or the P2X7R agonist BzATP. Assessments included airway hyperresponsiveness, histopathology, inflammatory cell counts, cytokine profiling (ELISA), flow cytometry for T-cell subsets, and protein analysis via western blot and immunofluorescence. Autophagy was evaluated by measuring LC3-I/II, Beclin-1, and acidic vesicular organelles. Key signaling molecules (P2X7R, NLRP3, ASC, caspase-1, LKB1/AMPK/mTOR) were analyzed. In vitro, ASMCs were treated with BzATP, PD, and specific inhibitors; P2X7R was silenced using siRNA.

resultsPD treatment significantly alleviated ovalbumin-induced airway hyperresponsiveness, inflammatory cell infiltration, goblet cell hyperplasia, and collagen deposition in mice. It restored the Th1/Th2 and Th17/Treg balance and reduced levels of airway remodeling markers (α-SMA, PCNA, VEGF, MMP-9). PD suppressed excessive autophagy (reduced LC3-I/II and Beclin-1) and modulated the LKB1/AMPK/mTOR pathway. Furthermore, PD inhibited the ATP/P2X7R axis, leading to reduced NLRP3 inflammasome activation, caspase-1 activity, and secretion of IL-1β and IL-18. In ASMCs, PD reversed BzATP-induced autophagy and NLRP3 activation. Silencing P2X7R enhanced AMPK phosphorylation, underscoring its role in the pathway.

conclusionPD attenuates airway remodeling in asthma by inhibiting the ATP/P2X7R-NLRP3 inflammasome axis and subsequent excessive autophagy, partly through modulation of the LKB1/AMPK/mTOR signaling pathway. These findings highlight PD as a promising therapeutic candidate for asthma treatment.

Indexed as

Airway RemodelingAsthmaAutophagyGlucosidesNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Purinergic P2X7StilbenesAnimalsDisease Models, AnimalInflammasomesMiceMice, Inbred BALB CMyocytes, Smooth MuscleOvalbuminSignal TransductionGlucosidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOvalbuminP2rx7 protein, mousepolydatinReceptors, Purinergic P2X7Stilbenesairway remodelingasthmaautophagyNLRP3P2X7Rpolydatin

Identifiers

PMID41937438
PMCPMC13051949

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.