Department of Pediatrics, Fujian Maternity and Child Health hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Central Laboratory of the First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
J Biol Regul Homeost Agents. 2020 Sep-Oct;34(5):1679-1688. doi: 10.23812/20-252-A.
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.
急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）是一种非常危险的疾病。本研究旨在探讨纤维生长因子-2（FGF-2）对脂多糖（LPS）诱导的肺损伤及其机制的影响。研究采用 C57/BL6 小鼠构建 LPS 诱导的 ALI/ARDS 模型，体外培养人正常肺上皮细胞系 BEAS-2B，探讨 FGF-2 对肺的作用及其作用机制。FGF-2 显著降低了小鼠肺湿/干重比、BALF 中细胞和炎症因子的数量以及肺组织中的髓过氧化物酶（MPO）活性。此外，FGF-2 还降低了小鼠肺组织中的氧化应激水平。在体外，FGF-2 有效降低了 LPS 诱导的 BEAS-2B 细胞的炎症和凋亡水平，并增加了 PI3K/Akt 信号通路的活性。然而，PI3K/Akt 信号通路的抑制剂 LY294002 减轻了 FGF-2 对肺组织的保护作用。因此，FGF-2 通过激活 PI3K/Akt 信号通路减轻肺泡上皮细胞的炎症、氧化应激和凋亡。
