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Volume 27, Issue 18
  • ISSN: 1386-2073
  • E-ISSN: 1875-5402

Abstract

Background

Bronchopulmonary dysplasia (BPD) is a chronic lung condition that occurs in premature infants who undergo prolonged mechanical ventilation and oxygen therapy. Existing treatment methods have shown limited efficacy, highlighting the urgent need for new therapeutic strategies. Artesunate (AS) is a compound known for its potential anti-inflammatory properties, and studies have shown its protective effects against acute lung injury. However, its impact on BPD and the underlying mechanisms remain unclear.

Objective

To investigate the effect and underlying mechanism of AS on chronic hyperoxia-induced BPD in neonatal mice.

Methods

Full-term C57BL/6J mice were randomly assigned to the Air+lactate Ringer's solution (L/R) group, O + L/R group, and O + AS group. Analysis was performed using assay methods such as ELISA, RT-qPCR, hematoxylin-eosin staining, and Western blotting.

Results

Compared with the O+L/R group, the expression of inflammatory factors in the serum, tissue, and BALF of the O+AS group was significantly reduced, the lung function of the mice was improved, and the inflammatory infiltrates were significantly alleviated. AS inhibited the mRNA expression of inflammatory factors in mice. We found that the expression of nuclear p65 and cytoplasmic p-IκBα in the NF-κB pathway was inhibited after adding AS.

Conclusion

AS ameliorated chronic hyperoxia-induced BPD in neonatal mice probably by inhibiting the expression of NF-κB pathway and inflammatory factors.

© 2024 Bentham Science Publishers
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2023-10-11
2025-01-13

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Artesunate Alleviates Chronic Hyperoxia-induced Bronchopulmonary Dysplasia by Suppressing NF-κB Pathway in Neonatal Mice
Comb Chem High Throughput Screen 27, 2681 (2024); https://doi.org/10.2174/0113862073246710231002042239
/content/journals/cchts/10.2174/0113862073246710231002042239
/content/journals/cchts/10.2174/0113862073246710231002042239
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  • Article Type:     Research Article
Keyword(s): Artesunate; bronchopulmonary dysplasia; inflammation; mice; mRNA expression; neonatal

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