PEDF inhibits LPS-induced acute lung injury in rats and promotes lung epithelial cell survival by upregulating PPAR-γ

• Published in: BMC pulmonary medicine 2023-09, Vol.23 (1), p.1-359, Article 359
• Main Authors: Xu, Lei, Chen, Yifei, Feng, Shoujie, Liu, Zeyan, Ye, Ying, Zhou, Ranran, Liu, Lijun
• Format: Article
• Language: English
• Subjects: ALI; Angiogenesis inhibitors; Anti-inflammatory; Antibodies; Apoptosis; Biotechnology; Cell injury; Cell survival; Cells; Epithelial cell; Epithelial cells; Epithelium; Fatalities; Inflammation; Laboratory animals; Lipopolysaccharides; Lungs; Medical prognosis; PEDF; Peroxisome proliferator-activated receptors; Pigment epithelium-derived factor; PPAR-γ; Proteins; Pulmonology; Tumor necrosis factor-TNF; Tumor necrosis factor-α
• ISSN: 1471-2466; 1471-2466
• DOI: 10.1186/s12890-023-02666-3

BackgroundThe progression of acute lung injury (ALI) involves numerous pathological factors and complex mechanisms, and cause the destruction of epithelial and endothelial barriers. Pigment epithelium-derived factor (PEDF) is an angiogenesis inhibitor and a potential anti-inflammatory factor. The purpose of this study was to investigate the effect of PEDF on lipopolysaccharide (LPS)-induced ALI in rats.MethodsIn vivo, pathological and injury related factors examination were performed on rat lung to investigate the effect of PEDF on ALI. In vitro, the effect of PEDF on inflammatory injury and apoptosis of lung epithelial type II RLE-6TN cell was evaluated, and the expression of inflammatory factors and related pathway proteins and PPAR-γ (in the presence or absence of PPAR-γ inhibitors) were analyzed.ResultsIn vivo results showed that PEDF inhibited the inflammatory factor expression (TNF-α, IL-6 and IL-1β) and progression of ALI and reduced lung cell apoptosis in rats. In vitro results showed that PEDF could effectively inhibit LPS-stimulated inflammatory damage and apoptosis of RLE-6TN cells. PEDF inhibited the RLE-6TN cell injury by enhancing the expression of PPAR-γ.ConclusionsPEDF is an anti-inflammatory factor, which can inhibit apoptosis of lung epithelial cells by upregulating the expression of PPAR-γ and reducing LPS-induced ALI in rats.