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

다국어 초록 (Multilingual Abstract)

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.

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