Background

Inflammation and oxidative stress-induced molecular death are one of the important causes for lung injury in critically ill patients. LKB1 is an important protein kinase in the body and has regulated inflammation and oxidative stress. However, LKB1 control inflammation and oxidative stress in lung injury were unclear.

Objective

We aimed to investigate the function and mechanism of Liver kinase B1 (LKB1) in lipopolysaccharide (LPS)-induced lung injury.

Result

LKB1 prevented lung injury, and weakened correlation oxidative stress and inflammatory reaction in LPS-induced mice model of lung injury. Up-regulation of LKB1 reduced reactive oxygen species (ROS) production and it-induced oxidative stress, and weakened inflammatory reactions in LPS-induced lung injury A549 cells. Down-regulation of LKB1 increased ROS production and it-induced oxidative stress, and enhanced inflammatory reactions in LPS-induced lung injury A549 cells. LKB1 induced phosphorylation (p)-AMPK protein expression, and suppressed the protein expression of NLRP3 in LPS-induced mice model of lung injury and in LPS-induced lung injury A549 cells. This experiment demonstrated the inhibition of AMPK or activation of NLRP3 inflammasome reversed the anti-inflammation function of LKB1 in LPS-induced lung injury. Meanwhile, ROS-induced oxidative stress also participated in the anti-inflammation effects of LKB1 in LPS-induced lung injury.

Conclusion

Therefore, our results indicate that LKB1 reduced inflammation and oxidative stress by regulating the AMPK/NLRP3 signaling pathway in LPS-induced lung injury.

中文翻译：

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肝激酶 B1 (LKB1) 通过调节 LPS 诱导的肺损伤中的 AMPK/NLRP3 信号通路减轻炎症和氧化应激

背景

炎症和氧化应激诱导的分子死亡是危重患者肺损伤的重要原因之一。LKB1 是体内重要的蛋白激酶，调节炎症和氧化应激。然而，LKB1 控制肺损伤中的炎症和氧化应激尚不清楚。

目标

我们旨在研究肝激酶 B1 (LKB1) 在脂多糖 (LPS) 诱导的肺损伤中的功能和机制。

结果

LKB1预防肺损伤，并减弱LPS诱导的肺损伤小鼠模型中氧化应激和炎症反应的相关性。LKB1 的上调减少了活性氧 (ROS) 的产生及其诱导的氧化应激，并减弱了 LPS 诱导的肺损伤 A549 细胞的炎症反应。LKB1 的下调增加了 ROS 的产生和它诱导的氧化应激，并增强了 LPS 诱导的肺损伤 A549 细胞的炎症反应。LKB1 诱导磷酸化 (p)-AMPK 蛋白表达，并抑制 LPS 诱导的肺损伤小鼠模型和 LPS 诱导的肺损伤 A549 细胞中 NLRP3 的蛋白表达。该实验证明抑制AMPK或激活NLRP3炎症小体逆转了LKB1在LPS诱导的肺损伤中的抗炎功能。同时，

结论

因此，我们的结果表明 LKB1 通过调节 LPS 诱导的肺损伤中的 AMPK/NLRP3 信号通路来减轻炎症和氧化应激。