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Fibroblast Growth Factor 21 dependent TLR4/MYD88/NF-κB signaling activation is involved in lipopolysaccharide-induced acute lung injury.

成纤维细胞生长因子 21 依赖的 TLR4/MYD88/NF-κ b 信号活化参与脂多糖诱导的急性肺损伤。

  • 影响因子:3.32
  • DOI:10.1016/j.intimp.2020.106219
  • 作者列表:"Gao J","Liu Q","Li J","Hu C","Zhao W","Ma W","Yao M","Xing L
  • 发表时间:2020-01-25
Abstract

: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.

摘要

: 据报道,成纤维细胞生长因子 21 (FGF21) 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生发展的重要机制。本研究评估 FGF21 预处理是否能缓解急性肺损伤。在脂多糖 (LPS) 处理之前用 FGF21 预处理小鼠。24 h 后取肺组织及 BALF,检测 H & E 病理、 W/D 比值、促炎因子 (TNF-α 、 il-1 β 和 IL-6) 及细胞凋亡。在体外,用 TLR4 或 MYD88 或 NF-κ b 质粒检测人 BEAS-2B 和 THP-1 细胞的炎症或凋亡。实验结果表明,FGF21 对 LPS 诱导的 Balb/c 小鼠或 LPS 诱导的 BEAS-2B 细胞和 THP-1 细胞有抑制炎症反应和凋亡的作用。此外,数据显示 FGF21 通过抑制 TLR4/MYD88/NF-κ b 信号通路抑制炎症和凋亡。因此,FGF21 为 LPS 诱导的急性肺损伤的治疗提供了可能。

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作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

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DOI:10.1042/BST20191010
作者列表:["Zaragosi LE","Deprez M","Barbry P"]

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