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Dapk1 promoted inflammation of infantile pneumonia by p38MAPK/NF-κB signaling pathway

机译:DAPK1通过P38MAPK / NF-κB信号通路促进了婴儿肺炎的炎症

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Background The present study was designed to investigate the function of death-associated protein kinase 1 (DAPK1) in infantile pneumonia and explore the potential mechanism of the actions. Objective Male C57BL/6 mice were injected with 2 mg/kg of LPS for the mice model of infantile pneumonia. A549 cells were treated with 100 ng/ml of LPS for vitro model of infantile pneumonia. Dapk1 mRNA and protein expressions in 6, 12 or 24 h after induction model of mice. Results Dapk1 gene increased inflammation in vitro model through activation of p38MAPK-mediated NF-κB expression. The inhibition of p38MAPK or NF-κB reduced the pro-inflammation effects of DAPK1 in infantile pneumonia. Conclusions Our study demonstrates that Dapk1 promoted inflammation of infantile pneumonia by p38MAPK/NF-κB signaling pathway, may be achieved inflammation by activation of p38MAPK/NF-κB signaling pathway.
机译:背景技术本研究旨在探讨死亡相关蛋白激酶1(DAPK1)在婴儿肺炎中的功能,并探讨该行动的潜在机制。 目的雄性C57BL / 6小鼠注射了2mg / kg LPS的婴儿肺炎的小鼠模型。 将A549细胞用100ng / ml LPS进行处理,用于婴儿肺炎的体外模型。 小鼠诱导模型后6,12或24小时的DAPK1 mRNA和蛋白质表达。 结果DAPK1基因通过P38MAPK介导的NF-κB表达激活增加体外模型的炎症。 P38MAPK或NF-κB的抑制减少了DAPK1在婴儿肺炎中的促炎作用。 结论我们的研究表明,DAPK1通过P38MAPK / NF-κB信号通路促进了婴儿肺炎的炎症,可以通过激活P38MAPK / NF-κB信号通路来实现炎症。

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