ArticleInternational journal of clinical and experimental pathology2018
Aspirin-triggered lipoxin A4 attenuates lipopolysaccharide-induced acute lung injury by inhibiting activation of mitogen-activated protein kinases and NF-κB in mice.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Acetylsalicylic acid and dihydroartemisinin combined therapy on experimental malaria-associated acute lung injury: analysis of lung function and the inflammatory process.Malaria journal · 2024Article
- Potential role of lipoxin in the management of COVID-19: a narrative review.Inflammopharmacology · 2022Review
- Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease.Frontiers in pharmacology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite advances in patient care, effective approaches to acute lung injury (ALI), are currently unceratin. Aspirin-triggered lipoxin A4 (ATL), an endogenous lipid mediator, has been found to have potent anti-inflammatory and pro-resolving effects. In this study, we found ATL exerted protective effects on LPS-induced ALI in mice through inhibiting activations of MAPKs and NF-κB. Our findings revealed that pretreatment by ATL alleviated lung histopathologic changes and injury scores, and reduced leukocytes and protein concentration in the bronchoalveolar lavage fluid (BALF). We further found down-regulation of pulmonary myeloperoxidase (MPO) activity, tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein (MCP)-1, and up-regulation of interleukin-10 levels after treatment with ATL in a dose-dependent manner. Moreover, ATL blocked phosphorylations of p38 MAPK, ERK1/2 and JNK, activation of NF-κB, and DNA-binding activity of activator protein-1 (AP-1) and NF-κB in the lung tissues of LPS-challenged mice. Our study suggested that the anti-inflammatory effects of ATL on LPS-induced ALI in mice were at least partly correlated with inhibited activations of mitogen-activated protein kinases and NF-κB.
Indexed as
Identifiers
31938370PMC6958252W3012221419What OpenQuestion holds
Registered trials
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.