Evidence map›Paper›PMID 38459479›Full record

ArticleBMC biotechnology2024

Polyphyllin B inhibited STAT3/NCOA4 pathway and restored gut microbiota to ameliorate lung tissue injury in cigarette smoke-induced mice.

Qing Wang, Zhiyi He, Jinqi Zhu, Mengyun Hu, Liu Yang, Hongzhong Yang

Open access · goldAbstract read
In one paragraph

Article in BMC biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  7. PMAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  10. Syringetin relieves bone cancer pain in rats induced by breast cancer cells through the ESR1/PRDM2 axis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

6 authors at 3 institutions in 1 country.

Qing WangThe Affiliated Changsha Central Hospital, Department of Respiratory and Critical Care Medicine, Hengyang Medical School, University of South China, Changsha, Hunan, 410004, China.
Zhiyi HeDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China.
Jinqi ZhuThe Affiliated Changsha Central Hospital, Department of Respiratory and Critical Care Medicine, Hengyang Medical School, University of South China, Changsha, Hunan, 410004, China.
Mengyun HuThe Affiliated Changsha Central Hospital, Department of Respiratory and Critical Care Medicine, Hengyang Medical School, University of South China, Changsha, Hunan, 410004, China.
Liu YangThe Affiliated Changsha Central Hospital, Department of Respiratory and Critical Care Medicine, Hengyang Medical School, University of South China, Changsha, Hunan, 410004, China.
Hongzhong YangThe Affiliated Changsha Central Hospital, Department of Respiratory and Critical Care Medicine, Hengyang Medical School, University of South China, Changsha, Hunan, 410004, China. 2018050665@usc.edu.cn.
University of South China · CNChangsha Central Hospital · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

Science and Technology Program Foundation of Changsha kq2202044Scientific Research Project of Hunan Provincial Department of Education 20C1591Scientific Research Project of Hunan Provincial Health Commission 202203022887
6 · The paper itself

Abstract

objectiveSmoking was a major risk factor for chronic obstructive pulmonary disease (COPD). This study plan to explore the mechanism of Polyphyllin B in lung injury induced by cigarette smoke (CSE) in COPD.

methodsNetwork pharmacology and molecular docking were applied to analyze the potential binding targets for Polyphyllin B and COPD. Commercial unfiltered CSE and LPS were used to construct BEAS-2B cell injury in vitro and COPD mouse models in vivo, respectively, which were treated with Polyphyllin B or fecal microbiota transplantation (FMT). CCK8, LDH and calcein-AM were used to detect the cell proliferation, LDH level and labile iron pool. Lung histopathology, Fe

resultsPolyphyllin B had a good binding affinity with STAT3 protein, which as a target gene in COPD. Polyphyllin B inhibited CS-induced oxidative stress, inflammation, mitochondrial damage, and ferritinophagy in COPD mice. 16S rRNA sequencing and FMT confirmed that Akkermansia and Escherichia_Shigella might be the potential microbiota for Polyphyllin B and FMT to improve CSE and LPS-induced COPD, which were exhausted by the antibiotics in C + L and C + L + P mice. CSE and LPS induced the decrease of cell viability and the ferritin and LC3 expression, and the increase of NCOA4 and p-STAT3 expression in BEAS-2B cells, which were inhibited by Polyphyllin B. Polyphyllin B promoted ferritin and LC3II/I expression, and inhibited p-STAT3 and NCOA4 expression in CSE + LPS-induced BEAS-2B cells.

conclusionPolyphyllin B improved gut microbiota disorder and inhibited STAT3/NCOA4 pathway to ameliorate lung tissue injury in CSE and LPS-induced mice.

Indexed as

Cigarette SmokingGastrointestinal MicrobiomeLung InjuryPulmonary Disease, Chronic ObstructiveAnimalsCell LineFerritinsInflammationLipopolysaccharidesLungMiceMolecular Docking SimulationRNA, Ribosomal, 16SSTAT3 Transcription FactorFerritinsLipopolysaccharidesRNA, Ribosomal, 16SSTAT3 Transcription FactorCigarette smokeCOPDGut microbiotaPolyphyllin BSTAT3/NCOA4 pathway

Identifiers

PMID38459479
PMCPMC10921762
OpenAlexW4392597090

What Socratic 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 Socratic graph.