Journal
MOLECULAR MEDICINE
Volume 26, Issue 1, Pages -Publisher
SPRINGER
DOI: 10.1186/s10020-020-00221-y
Keywords
FGF2; ALI; Inflammation; Permeability
Funding
- National Natural Science Foundation of China [81873949, 81671968, 8197894]
- Natural Science Foundation of Zhejiang Province of China [LY17H150003]
- Medical Innovation Discipline of Zhejiang Province (Critical Care Medicine, Y2015)
- Wenzhou Municipal Science and Technology Bureau [2018ZY002]
- medical and health research project of Zhejiang Province of China [WKJ-ZJ-1909]
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Background Acute lung injury (ALI), which is induced by numerous pathogenic factors, especially sepsis, can generate alveolar damage, pulmonary edema and vascular hyper-permeability ultimately leading to severe hypoxemia. Fibroblast growth factor-2 (FGF2) is an important member of the FGF family associated with endothelial cell migration and proliferation, and injury repairment. Here, we conducted this study aiming to evaluate the therapeutic effect of FGF2 in sepsis-induced ALI. Methods Recombinant FGF2 was abdominally injected into septic mice induced by cecal ligation and puncture (CLP), and then the inflammatory factors of lung tissue, vascular permeability and lung injury-related indicators based on protein levels and gene expression were detected. In vitro, human pulmonary microvascular endothelial cells (HPMEC) and mouse peritoneal macrophages (PMs) were challenged by lipopolysaccharides (LPS) with or without FGF2 administration in different groups, and then changes in inflammation indicators and cell permeability ability were tested. Results The results revealed that FGF2 treatment reduced inflammation response, attenuated pulmonary capillary leakage, alleviated lung injury and improved survival in septic mice. The endothelial injury and macrophages inflammation induced by LPS were inhibited by FGF2 administration via AKT/P38/NF-kappa B signaling pathways. Conclusion These findings indicated a therapeutic role of FGF2 in ALI through ameliorating capillary leakage and inflammation.
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