Evidence map›Paper›PMID 30221694›Full record

ArticleMolecular medicine reports2018

Role of the Rho/ROCK signaling pathway in the protective effects of fasudil against acute lung injury in septic rats.

Yu Wang, Xiaofeng Wang, Wei Liu, Lichun Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. 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
2.9field-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

15 citing papers in PubMed, 47 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

4 authors at 1 institution in 1 country.

Yu WangEmergency Department, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, P.R. China.
Xiaofeng WangEmergency Department, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, P.R. China.
Wei LiuEmergency Department, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, P.R. China.
Lichun ZhangEmergency Department, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, P.R. China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fasudil, which is primarily prescribed to treat cerebral vasospasm, may also inhibit systemic inflammation and prevent sepsis‑induced acute lung injury (ALI) in rats, although the mechanisms remain elusive. The purpose of the present study was to investigate the role of the rhodopsin (Rho)/Rho‑associated protein kinase (ROCK) signaling pathway in the protective effects of fasudil on ALI in septic rats. A total of 60 Wistar rats were pretreated with fasudil (30 mg/kg) through intraperitoneal injections 1 h prior to cecal ligation and puncture. Administration of fasudil led to reductions in polymorphonuclear neutrophil counts, and the protein concentrations of tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 in the bronchoalveolar lavage fluid of rats with sepsis‑induced ALI. The results demonstrated that fasudil decreased sepsis‑induced bacteremia. In addition, fasudil effectively reduced the Evans blue content, wet/dry lung weight ratio, lung injury score, and expression levels of malondialdehyde and myeloperoxidase. However, the superoxide dismutase activity in the lung tissue of the rats was increased. Activated caspase‑3 activity in lung tissue was reduced to 29% by fasudil. Furthermore, the expression of Rho and ROCK1 was significantly downregulated, and the phosphorylation of myosin phosphatase‑targeting subunit 1 in lung tissues was markedly decreased, whereas the protein expression levels of zonula occludens 1 were increased in fasudil‑treated rats (P<0.05). In the in vitro experiments, vascular endothelial growth factor, intracellular adhesion molecule 1 and vascular cell adhesion molecule 1 secreted from human pulmonary microvascular endothelial cells treated with lipopolysaccharide (LPS) were attenuated by fasudil. Fasudil also reduced the fluorescence intensity of filamentous actin induced by LPS. Taken together, the results of the present study demonstrated that fasudil was able to improve endothelial permeability and inhibit inflammation, oxidative stress and cellular apoptosis in order to alleviate ALI in septic rats through inhibition of the Rho/ROCK signaling pathway.

Indexed as

1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAcute Lung InjuryAnimalsApoptosisBronchoalveolar Lavage FluidEndothelial CellsHumansInflammationLipopolysaccharidesOxidative StressRatsrho-Associated KinasesSepsis1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinefasudilLipopolysaccharidesrho-Associated Kinases

Identifiers

PMID30221694
PMCPMC6172402
OpenAlexW2889552347

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.