ArticleMolecular biology reports2011
Troglitazone-activated PPARγ inhibits LPS-induced lung alveolar type II epithelial cells injuries via TNF-α.
Article in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- The therapeutic efficacy of resveratrol for acute lung injury-A meta-analysis of preclinical trials.Frontiers in pharmacology · 2022Pooled it
- Analyses of alveolar epithelial injury via lipid-related stress in mammalian target of rapamycin inhibitor-induced lung disease.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- The Role of SIRT1 in Autophagy in Lipopolysaccharide-Induced Mouse Type II Alveolar Epithelial Cells.Inflammation · 2018Article
- GLP-1 Analogue Liraglutide Enhances SP-A Expression in LPS-Induced Acute Lung Injury through the TTF-1 Signaling Pathway.Mediators of inflammation · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are common syndromes characterized by diffuse, acute injury to the alveolar epithelium and pulmonary vascular endothelial cells, with high mortality rate for there are no effective pharmacological therapies. Peroxisome proliferators-activated receptor γ (PPARγ), a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors, is ubiquitously expressed within the lung. Recent studies have indicated PPARγ can protect lung tissue and alleviate pulmonary inflammatory injury. But no studies examined whether PPARγ agonists can protect the alveolar epithelial cells cultured in vitro. We observed the protective effect of PPARγ in LPS-induced alveolar type II epithelial cells injury. The results showed troglitazone-activated PPARγ could inhibit the production of TNF-α, one of the most important inflammatory factors, and then increased the expression of surfactant-associated protein A (SP-A) and attenuate the apoptosis of alveolar type II epithelial cells. Our results suggest that PPARγ may have a potential therapeutic effect on ALI.
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Registered trials
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