ArticleAmerican journal of translational research2021
Edaravone attenuates smoke inhalation injury in rats by the Notch pathway.
Article in American journal of translational research, 2021. 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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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Notch 2 from bone marrow mesenchymal stem cells alleviates smoke inhalation-induced lung injury by mediating alveolar cell differentiation.Journal of molecular histology · 2025Article
- Pirfenidone alleviates smoke inhalation lung injury of rats via the NF-κB signaling pathway.Immunity, inflammation and disease · 2024Article
- Edaravone: A Possible Treatment for Acute Lung Injury.International journal of general medicine · 2024Review
- Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the protective effect of inhaled edaravone (EDA) on inflammation, oxidative stress (OS), and pulmonary function (PF) in rats after smoke inhalation injury (SII), as well as its mechanisms.
methodsTwenty-four rats were designated as group A (model group), group B (EBA prevention group), group C (low-dose group) and group D (high-dose group) (n=6 for each group). SII models were induced in all groups. After successful modeling, rats in each group were treated accordingly. After 6 hours of modeling, assessments of PF, oxygenation index (OI), inflammatory cytokine expression, oxidative stress index (OSI), wet/dry weight ratio (W/D), total lung water (TLW), and the expression of Notch markers were carried out.
resultsCompared with group A, the remaining groups had higher peak respiratory velocity (PEF), forced expiratory volume in the first second (FEV1), FEV1/forced vital capacity (FVC) and OI, as well as lower W/D and TLW; levels of serum superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 decreased, and those of serum myeloperoxidase (MPO) and IL-10 increased. Levels of PEF, FEV1, FVC, OI, MPO, and IL-10 were higher in group A than in groups C and D, and those of W/D, TLW, SOD, MDA, TNF-α, and IL-6 were lower. Levels of Notch markers NICD, Hes1 and Hes5 were downregulated in groups B, C, and D, and in group B were lower than those in groups C and D.
conclusionInhaled EDA is able to alleviate inflammation and OS and effectively improve PF in rats after SII, possibly by inhibiting the Notch pathway.
Indexed as
Identifiers
34150051PMC8205801W3175330050What 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.