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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WZ: guarantor of integrity of the entire study, study concepts and design, definition of intellectual content, clinical studies, manuscript review; WZ: study design, literature research, experimental studies, data acquisition and analysis, statistical analysis, manuscript preparation; WZ: experimental studies; WZ: data acquisition and analysis; WZ: manuscript preparation and editing.
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This study was approved by the Ethics committee of the Affiliated Changzhou NO.2 People’s Hospital of Nanjing Medical University.
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Zhang, W. Dapk1 promoted inflammation of infantile pneumonia by p38MAPK/NF-κB signaling pathway. Mol. Cell. Toxicol. 17, 297–304 (2021). https://doi.org/10.1007/s13273-021-00136-7
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DOI: https://doi.org/10.1007/s13273-021-00136-7