Evidence map›Paper›PMID 27412237›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

CORM-2 inhibits TXNIP/NLRP3 inflammasome pathway in LPS-induced acute lung injury.

Lei Jiang, Dongsheng Fei, Rui Gong, Wei Yang, Wei Yu, Shangha Pan, Mingran Zhao, Mingyan Zhao

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 71 citations in OpenAlex.

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    Review
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  15. Article
  16. Review
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  18. S1P/S1PAntioxidants (Basel, Switzerland) · 2021
    Article
  19. Review
  20. Review
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

8 authors at 2 institutions in 1 country.

Lei JiangDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China.
Dongsheng FeiDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China.
Rui GongDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China.
Wei YangDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China.
Wei YuDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China.
Shangha PanThe Key Hepatosplenic Surgery Laboratory, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Mingran ZhaoDepartment of Pediatrics, Children's Hospital of Harbin City, Harbin, China.
Mingyan ZhaoDepartment of ICU, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang province, China. mingyan1970@126.com.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAccumulated studies suggest that exogenously administered carbon monoxide is beneficial for the resolution of acute lung inflammation. The present study aimed to examine the effects and the underlying mechanisms of CORM-2 on thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway in lipopolysaccharide (LPS)-induced acute lung injury (ALI).

methodsALI was intratracheally induced by LPS in C57BL6 mice. CORM-2 or iCORM-2 (30mg/kg i.p.) was administered immediately before LPS instillation. 6 h later, lung bronchoalveolar lavage (BAL) fluids were acquired for IL-18, IL-1β, and cell measurement, and lung issues were collected for histologic examination, wet/dry weight ratio, and determination of TXNIP/NLRP3 inflammasome expression, NLRP3 inflammasome and NF-ΚB activity, and reactive oxygen species (ROS) production.

resultsLPS triggered significant lung edema, lung injury, and leukocyte infiltration, and elevated the levels of IL-1β and IL-18 in lung BAL fluids. CORM-2 pretreatment resulted in a marked amelioration of lung injury and reduced IL-1β and IL-18 secretion in BAL fluids. In lung tissues; CORM-2 down-regulated mRNA and protein level of TXNIP, NLRP3, ASC, and caspase-1. Furthermore, CORM-2 reduced ROS production, inhibited NLRP3 inflammasome and NF-κB activity, and interaction of TXNIP-NLRP3. However, no significant differences were detected between the LPS and iCORM-2 (an inactive variant of CORM-2) group.

conclusionCORM-2 suppresses TXNIP/NLRP3 inflammasome pathway and protects against LPS-induced lung injury.

Indexed as

Acute Lung InjuryAnimalsAnti-Inflammatory AgentsBronchoalveolar Lavage FluidCarrier ProteinsCaspase 1InflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesLungMaleMice, Inbred C57BLNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOrganometallic CompoundsAnti-Inflammatory AgentsCarrier ProteinsCaspase 1InflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOrganometallic CompoundsPeroxidaseReactive Oxygen SpeciesThioredoxinstricarbonyldichlororuthenium (II) dimerTxnip protein, mouseAcute lung injuryCarbon monoxideNLRP3 inflammasomeTXNIP

Identifiers

PMID27412237
OpenAlexW2462051602

What OpenQuestion holds

Textmetadata
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.