Evidence map›Paper›PMID 32750045›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Role and Mechanism of Maresin-1 in Acute Lung Injury Induced by Trauma-Hemorrhagic Shock.

Huayi Ma, Song Mo, Qushen Yi, Junhua Lai, Huan Liu, Zhanying Shi

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Mechanism of Phosgene-Induced Acute Lung Injury and Treatment Strategy.International journal of molecular sciences · 2021
    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

6 authors at 2 institutions in 1 country.

Huayi MaDepartment of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland).
Song MoDepartment of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland).
Qushen YiDepartment of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland).
Junhua LaiDepartment of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland).
Huan LiuDepartment of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland).
Zhanying ShiLiuzhou Worker's Hospital, Liuzhou, Guangxi, China (mainland).
Fourth Affiliated Hospital of Guangxi Medical University · CNLiuzhou General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND It is reported that trauma hemorrhagic shock (THS) could resulted in organ injury and is related to a high mortality rate. Maresin-1 (MaR1), a derived medium through biosynthesis, is involved in inflammatory responses. However, the mechanism of MaR1 against acute lung injury needs to be further understood. This report aimed to explore whether MaR1 had a protective effect on lung injury. MATERIAL AND METHODS We constructed a THS-induced acute lung damage rat model and then treated the rats with MaR1. We determined Evan's blue dye (EBD) lung permeability, lung permeability index, wet/dry (W/D) weight ratio, nitric oxide (NO) concentration and inducible nitric oxide synthase (iNOS) expression in lung tissue samples. The inflammation-related cytokines levels in the bronchoalveolar lavage fluid (BALF) and serum of rats were determined by enzyme-linked immunosorbent assay (ELISA). Finally, the TLR4/p38MAPK/NF-kappaB pathway was analyzed by quantitative real-time polymerase chain reaction and western blot assay. RESULTS The increased EBD ratio, lung permeability index and W/D weight ratio, NO concentration and iNOS levels were suppressed by MaR1 treatment. THS-induced over-production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in BALF and serum was suppressed by MaR1. Besides, the TLR4/p38MAPK/NF-kappaB pathway activation in THS-induced rats were inhibited by MaR1 treatment. CONCLUSIONS Our study showed that MaR1 could effectively alleviated THS-induced lung injury via inhibiting the excitation of the TLR4/p38MAPK/NF-kappaB pathway in THS-induced rats, suggesting that MaR1 might be a novel agent for lung damage treatment.

Indexed as

Acute Lung InjuryAnimalsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalDocosahexaenoic AcidsInflammationMaleNF-kappa BNitric OxideNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesProtective AgentsRatsRats, Sprague-DawleyShock, Hemorrhagic7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acidCytokinesDocosahexaenoic AcidsNF-kappa BNitric OxideNitric Oxide Synthase Type IINos2 protein, ratp38 Mitogen-Activated Protein KinasesProtective AgentsTlr4 protein, ratToll-Like Receptor 4

Identifiers

PMID32750045
PMCPMC7427347
OpenAlexW3047756990

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.