ArticleIranian journal of basic medical sciences2015
Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats.
Article in Iranian journal of basic medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Transplanted MSCs promote alveolar bone repair via hypoxia-induced extracellular vesicle secretion.Oral diseases · 2024Article
- Bioactive phenolics fraction ofHeliyon · 2022Article
- Visfatin Exerts Immunotherapeutic Effects in Lipopolysaccharide-Induced Acute Lung Injury in Murine Model.Inflammation · 2020Article
- Traditional Applications, Phytochemistry, and Pharmacological Activities ofFrontiers in pharmacology · 2020Review
- Expression levels and significance of miR-184 and miR-126 in burned rats.Experimental and therapeutic medicine · 2019Article
- Celecoxib Protects Hyperoxia-Induced Lung Injury via NF-κB and AQP1.Frontiers in pediatrics · 2019Article
- Chelerythrine Attenuates the Inflammation of Lipopolysaccharide-Induced Acute Lung Inflammation Through NF-κB Signaling Pathway Mediated by Nrf2.Frontiers in pharmacology · 2018Article
- Effects of sevoflurane preconditioning on lung injury during one lung ventilation.International journal of clinical and experimental medicine · 2015Article
- Role of Sphingolipids in the Pathobiology of Lung Inflammation.Mediators of inflammation · 2015Review
Corrections and comments
- Retraction · 2019-09-25Date of Article and/or Notice Unknown · False/Forged Authorship · Lack of Approval from Author · · retraction date unknown, estimated from notifications
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTherapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI). MATERIALS AND
methodsIn this study, we investigated the time course changes of oxidative stress and inflammation in lung tissues of rats exposed to >95% oxygen for 12-60 hr.
resultsWe found that at 12 hr after hyperoxia challenge, the activities of superoxide dismutase and glutathione peroxidase were significantly reduced with remarkably increased lipid peroxidation. At 12 hr, NF-κB p65 expression was also upregulated, but Iκ-Bα expression showed a remarkable decline. Significant production of inflammatory mediators, e.g, interleukin-1β, occurred 24 hr after hyperoxia exposure. In addition, the expression of intracellular adhesion molecule 1 expression and the activity of myeloperoxidase were significantly increased at 24 hr with a peak at 48 hr.
conclusionOur data support that hyperoxia-induced oxidative damage and NF-κB pathway activation implicate in the early phase of HALI pathogenesis.
Indexed as
Identifiers
25810882PMC4366750W1559070201What 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.