Quercetin alleviates hyperoxia-induced bronchopulmonary dysplasia by inhibiting ferroptosis through the MAPK/PTGS2 pathway: Insights from network pharmacology, molecular docking, and experimental evaluations

  • Chem Biol Drug Des. 2024 Apr;103(4):e14520. doi: 10.1111/cbdd.14520.
Xianhui Deng  1 ,  Dan Chen  2 ,  Anni Xie  1 ,  Shengpeng Li  2 ,  Ailing Chen  3 ,  Qin Zhou  1  4 ,  Renqiang Yu  1  3
Affiliations
  • 1. Department of Neonatology, Affiliated Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China.
  • 2. Department of Physiopathology, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
  • 3. Research Institute for Reproductive Health and Genetic Diseases, Affiliated Women's Hospital of Jiangnan University, Wuxi, China.
  • 4. Department of Pediatric, Wuxi Yihe Gynaecology and Obstetrics Hospital, Wuxi, China.
PMID: 38570710 DOI: 10.1111/cbdd.14520
Abstract

Quercetin, a bioactive natural compound renowned for its potent anti-inflammatory, antioxidant, and Antiviral properties, has exhibited therapeutic potential in various diseases. Given that bronchopulmonary dysplasia (BPD) development is closely linked to inflammation and oxidative stress, and quercetin, a robust antioxidant known to activate NRF2 and influence the Ferroptosis pathway, offers promise for a wide range of age groups. Nonetheless, the specific role of quercetin in BPD remains largely unexplored. This study aims to uncover the target role of quercetin in BPD through a combination of network pharmacology, molecular docking, computer analyses, and experimental evaluations.

Keywords
PTGS2; bronchopulmonary dysplasia; ferroptosis; hyperoxia; quercetin.
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