Evidence map›Paper›PMID 35962798›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022

Proteomic analysis and identification reveal the anti-inflammatory mechanism of clofazimine on lipopolysaccharide-induced acute lung injury in mice.

Bo Yang, Zhan Gao, Qi-Shuang Li, Xiang-Ye Zhang, Lan Song, Yi-Ni Wang, Xin-Yue Wang, Lin-Lin Ji, Hong-Liang Xu, Hui Xie and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

15 authors at 5 institutions in 1 country.

Bo Yang *Department of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China.
Zhan Gao *State Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Qi-Shuang Li *State Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Xiang-Ye Zhang *State Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Lan SongState Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Yi-Ni WangState Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Xin-Yue WangState Key Laboratory of Proteomics, Beijing Proteome Research Center, Institute of Lifeomics, National Center for Protein Sciences, Beijing, 102206, People's Republic of China.
Lin-Lin JiDepartment of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China.
Hong-Liang XuDepartment of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China.
Hui XieDepartment of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China.
Fu-Kai FengDepartment of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China.
Xiao-Ping LiDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, 300192, People's Republic of China.
Wei LiDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, 300192, People's Republic of China.
Rong WangState Key Laboratory of Reliability and Intelligence of Electrical Equipment, Hebei University of Technology, Beichen District, Tianjin, 300401, People's Republic of China. rongwang@hebut.edu.cn.
Guang-Shun WangDepartment of Thoracic Surgery, Tianjin Baodi Hospital, Baodi Clinical College, Tianjin Medical University, Guangchuan Road, Baodi District, Tianjin, 301800, People's Republic of China. wgs@bddhospital.com.
Tianjin Medical University · CNBeijing Proteome Research Center · CNHebei University · CNHebei University of Technology · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveAcute lung injury (ALI)/ acute respiratory distress syndrome (ARDS) was increasingly recognized as one of the most severe acute hyperimmune response of coronavirus disease 2019 (COVID-19). Clofazimine (CFZ) has attracted attention due to its anti-inflammatory property in immune diseases as well as infectious diseases. However, the role and potential molecular mechanism of CFZ in anti-inflammatory responses remain unclear.

methodsWe analyze the protein expression profiles of CFZ and LPS from Raw264.7 macrophages using quantitative proteomics. Next, the protective effect of CFZ on LPS-induced inflammatory model is assessed, and its underlying mechanism is validated by molecular biology analysis.

resultsLC-MS/MS-based shotgun proteomics analysis identified 4746 (LPS) and 4766 (CFZ) proteins with quantitative information. The key proteins and their critical signal transduction pathways including TLR4/NF-κB/HIF-1α signaling was highlighted, which was involved in multiple inflammatory processes. A further analysis of molecular biology revealed that CFZ could significantly inhibit the proliferation of Raw264.7 macrophages, decrease the levels of TNF-α and IL-1β, alleviate lung histological changes and pulmonary edema, improve the survival rate, and down-regulate TLR4/NF-κB/HIF-1α signaling in LPS model.

conclusionThis study can provide significant insight into the proteomics-guided pharmacological mechanism study of CFZ and suggest potential therapeutic strategies for infectious disease.

Indexed as

Acute Lung InjuryCOVID-19 Drug TreatmentRespiratory Distress SyndromeAnimalsAnti-Inflammatory AgentsChromatography, LiquidClofazimineLipopolysaccharidesLungMiceNF-kappa BProteomicsTandem Mass SpectrometryToll-Like Receptor 4Anti-Inflammatory AgentsClofazimineLipopolysaccharidesNF-kappa BToll-Like Receptor 4Acute lung injuryAcute respiratory distress syndromeAnti-inflammatoryClofazimineLipopolysaccharideProteomics

Identifiers

PMID35962798
PMCPMC9376043
OpenAlexW4291222678

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.