成纤维细胞生长因子 21 依赖性 TLR4/MYD88/NF-κB 信号激活参与脂多糖诱导的急性肺损伤。
Fibroblast Growth Factor 21 dependent TLR4/MYD88/NF-κB signaling activation is involved in lipopolysaccharide-induced acute lung injury.
机构信息
Department of Respiratory Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450000, China.
Department of Respiratory Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450000, China.
出版信息
Int Immunopharmacol. 2020 Mar;80:106219. doi: 10.1016/j.intimp.2020.106219. Epub 2020 Jan 25.
Fibroblast Growth Factor 21 (FGF21) has been reported to reduce inflammation and apoptosis. Inflammation and apoptosis are both the essential mechanisms during development of acute lung injury. This study evaluated whether pre-treatment of FGF21 could alleviate acute lung injury. Mice were pre-treated with FGF21 prior to lipopolysaccharide (LPS) treatment. 24 h later, the lung tissues and BALF were obtained to detect H&E pathology, W/D ratio, pro-inflammatory factors (TNF-α, IL-1β and IL-6) and apoptosis. In vitro, Human BEAS-2B and THP-1 cells were overexpressed with TLR4 or MYD88 or NF-κB plasmid to detect the inflammation or apoptosis. Data showed that FGF21 was proved to be beneficial for inhibiting inflammation and apoptosis in the LPS- induced Balb/c mice or LPS induced BEAS-2B or THP-1 cells. Furthermore, the data showed that FGF21 suppressed inflammation and apoptosis via inhibition of TLR4/MYD88/NF-κB signaling pathway. Therefore, FGF21 provides a possibility for the treatment of LPS induced acute lung injury.
成纤维细胞生长因子 21（FGF21）已被报道可减轻炎症和细胞凋亡。炎症和细胞凋亡都是急性肺损伤发展过程中的关键机制。本研究评估了 FGF21 的预处理是否可以减轻急性肺损伤。在脂多糖（LPS）处理前，用 FGF21 预处理小鼠。24 小时后，获取肺组织和 BALF 以检测 H&E 病理学、W/D 比、促炎因子（TNF-α、IL-1β 和 IL-6）和细胞凋亡。在体外，人 BEAS-2B 和 THP-1 细胞过表达 TLR4 或 MYD88 或 NF-κB 质粒，以检测炎症或细胞凋亡。结果表明，FGF21 可抑制 LPS 诱导的 Balb/c 小鼠或 LPS 诱导的 BEAS-2B 或 THP-1 细胞中的炎症和细胞凋亡。此外，数据表明 FGF21 通过抑制 TLR4/MYD88/NF-κB 信号通路抑制炎症和细胞凋亡。因此，FGF21 为治疗 LPS 诱导的急性肺损伤提供了一种可能。
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