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

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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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Acknowledgements

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Authors and Affiliations

Authors

Contributions

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.

Corresponding author

Correspondence to Wenbo Zhang.

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Conflict of interest

There are no potential conflicts of interest to disclose.

Ethical approval

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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All patients have given their written informed consent.

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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

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