ArticleSaudi journal of biological sciences2022
Protective effect of Apremilast against LPS-induced acute lung injury via modulation of oxidative stress and inflammation.
Article in Saudi journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Apremilast ameliorates methotrexate-induced renal injury in rats: role of TLR4/NF-κB/P38 MAPK/caspase-3 and Nrf2/HO-1 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Exosomal cytokine profile on lipopolysaccharide-induced acute lung injury in mice.Journal of molecular histology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung injuries are attributed due to exposure to Drugs or chemicals. One of the important challenging situations for the clinicians is to manage treatments of different diseases with acute lung injury (ALI). The objective of this study was to investigate the possible protective mechanisms and action of a novel Phosphodiesterase-4 inhibitor "Apremilast" (AP) in lipopolysaccharide (LPS)-induced lung injury. Blood sample from each animals were collected in a vacuum blood collection tube. The rat lungs were isolated for oxidative stress assessment, western blot analysis and their mRNA expressions using RT-PCR. Exposure of LPS in rats causes significant increase in oxidative stress, activates the pro-inflammatory cytokines release like tissue necrotic factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), modulated gene expression, protein expression and histopathological changes which were reversed by administration of AP. Finding of the research enlighten the protective role of AP against LPS-induced ALI.
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Registered trials
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