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Fibrogrowth factor-2 protects against acute lung injury by activating the PI3K/Akt signaling pathway
Vol 34, Issue 5, 2020
Abstract
Acute lung injury (ALI)/Acute respiratory distress syndrome (ARDS) is a very dangerous disease. The purpose of this study was to investigate the effects of fibrogrowth factor-2 (FGF-2) on lipopolysaccharide (LPS)-induced lung injury and its mechanisms. C57/BL6 mice were used in the study and LPS was used to construct the ALI/ARDS model. In addition, human normal lung epithelial cell line BEAS-2B was cultured to investigate the effect of FGF-2 on the lung and its mechanism of action in vitro. FGF-2 significantly reduced wet/dry weight ratio of mice, the number of cells and inflammatory factors in BALF, and MPO activity in lung tissue. In addition, FGF-2 also reduced the level of oxidative stress in mouse lung tissue. In vitro, FGF-2 effectively reduced LPS-induced inflammatory and apoptotic levels of BEAS-2B cells and increased the activity of the PI3K/Akt signaling pathway. However, LY294002, an inhibitor of the PI3K/Akt signaling pathway, alleviated the protective effect of FGF-2 on lung tissue. Therefore, FGF-2 attenuated inflammation, oxidative stress and apoptosis in alveolar epithelial cells by activating the PI3K/Akt signaling pathway.
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Copyright (c) 2020 Q-Y. Tang, J-X. Wei, S-F. Xue, G-H. Liu, L-X. Fu
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy