ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Protection against LPS-induced acute lung injury by a mechanism-based inhibitor of NADPH oxidase (type 2).
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- Circadian Control of Pulmonary Endothelial Signaling Occurs via the NADPH Oxidase 2-NLRP3 Pathway.Journal of biological rhythms · 2025Article
- Effect of Acute Lung Injury (ALI) Induced by Lipopolysaccharide (LPS) on the Pulmonary Pharmacokinetics of an Antibody.Antibodies (Basel, Switzerland) · 2025Article
- Dose-dependent multi-organ injury following lipopolysaccharide gas inhalation.The Journal of international medical research · 2024Article
- Decreased LPS-induced lung injury in pigs treated with a lung surfactant protein A-derived nonapeptide that inhibits peroxiredoxin 6 activity and subsequent NOX1,2 activation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- Deuterated Arachidonic Acid Ameliorates Lipopolysaccharide-Induced Lung Damage in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Inhibition of Peroxiredoxin 6 PLA2 Activity Decreases Oxidative Stress and the Severity of Acute Lung Injury in the Mouse Cecal Ligation and Puncture Model.Antioxidants (Basel, Switzerland) · 2021Article
- A Peptide Inhibitor of Peroxiredoxin 6 Phospholipase AAntioxidants (Basel, Switzerland) · 2021Article
- Review
- Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37.International journal of molecular sciences · 2020Article
- Peroxiredoxins and Beyond; Redox Systems Regulating Lung Physiology and Disease.Antioxidants & redox signaling · 2019Review
- Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages.Bioscience reports · 2019Article
- A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS).International journal of molecular sciences · 2019Article
- Genetic inactivation of the phospholipase AAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Peroxiredoxin6 in Endothelial Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- Lipoxin A4 Ameliorates Acute Pancreatitis-Associated Acute Lung Injury through the Antioxidative and Anti-Inflammatory Effects of the Nrf2 Pathway.Oxidative medicine and cellular longevity · 2019Article
- Mitochondrial Division Inhibitor 1 Attenuates Mitophagy in a Rat Model of Acute Lung Injury.BioMed research international · 2019Article
- Identification of Small Peptides that Inhibit NADPH Oxidase (Nox2) Activation.Antioxidants (Basel, Switzerland) · 2018Article
- The Role of Peroxiredoxin 6 in Cell Signaling.Antioxidants (Basel, Switzerland) · 2018Review
- Detection of hydrogen peroxide production in the isolated rat lung using Amplex red.Free radical research · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The phospholipase A2 activity of peroxiredoxin 6 is inhibited by the transition state analog, 1-hexadecyl-3-(trifluoroethyl)-sn-glycero-2-phosphomethanol (MJ33). This activity is required for the activation of NADPH oxidase, type 2. The present study evaluated the effect of MJ33 on manifestations of acute lung injury. Mice were injected intratracheally (IT) with LPS from Escherichia coli 0111:B4 (LPS, 1 or 5 mg/kg), either concurrently with LPS or 2 h later, and evaluated for lung injury 24 h later. MJ33 inhibited reactive oxygen species (ROS) generation by lungs when measured at 24 h after LPS. LPS at either a low or high dose significantly increased lung infiltration with inflammatory cells, secretion of proinflammatory cytokines (IL-6, TNF-α, and the chemokine macrophage inflammatory protein-2), expression of lung vascular cell adhesion molecule, lung permeability (protein in bronchoalveolar lavage fluid, leakage of FITC-dextran, lung wet-to-dry weight ratio), tissue lipid peroxidation (thiobarbituric acid reactive substances, 8-isoprostanes), tissue protein oxidation (protein carbonyls), and activation of NF-κB. MJ33, given either concurrently or 2 h subsequent to LPS, significantly reduced all of these measured parameters. Previous studies of toxicity showed a high margin of safety for MJ33 in the intact mouse. Thus we have identified MJ33 as a potent, nontoxic, and specific mechanism-based inhibitor of NADPH oxidase type 2-mediated ROS generation that protects mice against lung injury associated with inflammation.
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