Evidence map›Paper›PMID 38730387›Full record

ArticleBMC pulmonary medicine2024

Sinomenine attenuates pulmonary fibrosis by downregulating TGF-β1/Smad3, PI3K/Akt and NF-κB signaling pathways.

Fuqiang Yao, Minghao Xu, Lingjun Dong, Xiao Shen, Yujie Shen, Yisheng Jiang, Ting Zhu, Chu Zhang, Guangmao Yu

Abstract read
In one paragraph

Article in BMC pulmonary medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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  10. Stem cell therapy targets THBS1 to reverse endometrial fibrosis.Frontiers in cell and developmental biology · 2026
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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

9 authors.

Fuqiang Yao *Department of Thoracic Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang, China.
Minghao Xu *School of Medicine, ShaoXing University, Shaoxing, Zhejiang, China.
Lingjun Dong *Department of Thoracic Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang, China.
Xiao ShenSchool of Medicine, ShaoXing University, Shaoxing, Zhejiang, China.
Yujie ShenSchool of Medicine, ShaoXing University, Shaoxing, Zhejiang, China.
Yisheng JiangSchool of Medicine, ShaoXing University, Shaoxing, Zhejiang, China.
Ting ZhuDepartment of Thoracic Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang, China.
Chu ZhangDepartment of Thoracic Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang, China.
Guangmao YuDepartment of Thoracic Surgery, Shaoxing People's Hospital, Shaoxing, Zhejiang, China. sxygmys@163.com.

Funding

he Zhejiang Provincial Medical and Health Science and Technology Plan Project 2023KY346Shaoxing People's Hospital Youth Scientific Research Fund Project 2023YB07Shaoxing People's Hospital Youth Scientific Research Fund Project 2023YB28the Zhejiang Provincial Medical and Health Science and Technology Plan Project 2020KY321
6 · The paper itself

Abstract

backgroundSince COVID-19 became a global epidemic disease in 2019, pulmonary fibrosis (PF) has become more prevalent among persons with severe infections, with IPF being the most prevalent form. In traditional Chinese medicine, various disorders are treated using Sinomenine (SIN). The SIN's strategy for PF defense is unclear.

methodsBleomycin (BLM) was used to induce PF, after which inflammatory factors, lung histological alterations, and the TGF-/Smad signaling pathway were assessed. By administering various dosages of SIN and the TGF- receptor inhibitor SB-431,542 to human embryonic lung fibroblasts (HFL-1) and A549 cells, we were able to examine proliferation and migration as well as the signaling molecules implicated in Epithelial-Mesenchymal Transition (EMT) and Extra-Cellular Matrix (ECM).

resultsIn vivo, SIN reduced the pathological changes in the lung tissue induced by BLM, reduced the abnormal expression of inflammatory cytokines, and improved the weight and survival rate of mice. In vitro, SIN inhibited the migration and proliferation by inhibiting TGF-β1/Smad3, PI3K/Akt, and NF-κB pathways, prevented the myofibroblasts (FMT) of HFL-1, reversed the EMT of A549 cells, restored the balance of matrix metalloenzymes, and reduced the expression of ECM proteins.

conclusionSIN attenuated PF by down-regulating TGF-β/Smad3, PI3K/Akt, and NF-κB signaling pathways, being a potential effective drug in the treatment of PF.

Indexed as

MorphinansProto-Oncogene Proteins c-aktPulmonary FibrosisSignal TransductionA549 CellsAnimalsBleomycinCell MovementCell ProliferationDisease Models, AnimalDown-RegulationEpithelial-Mesenchymal TransitionHumansLungMaleMiceBleomycinMorphinansNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktsinomenineSmad3 ProteinTransforming Growth Factor beta1Extracellular matrixNF-κBPI3K/AktPulmonary fibrosisSinomenineTGF-β1/Smad3

Identifiers

PMID38730387
PMCPMC11088103

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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.