Network pharmacology analysis and experimental validation elucidate the protective mechanisms of BYHWD against hypoxia/reoxygenation-induced endothelial cell injury
BYHWD may alleviate H/R-induced endothelial cell injury by suppressing oxidative stress and apoptosis through active components such as luteolin and quercetin, which target key genes including VEGFA and AKT1, thereby activating the PI3K/AKT/FOXO1 signaling pathway. This study provides integrated experimental evidence from network pharmacology, <i>in vitro</i>, and <i>in vivo</i> studies, supporting the use of BYHWD in AKI treatment.
Authors
- Yan Shi (ORCID: https://orcid.org/0000-0002-4336-0650)
- Yanyan Zhao (ORCID: https://orcid.org/0000-0002-1828-5038)
- Yuling Sun (ORCID: https://orcid.org/0000-0001-5289-4673)
- Qiancheng Zhu (ORCID: https://orcid.org/0000-0001-5480-1434)
- Lu Liu (ORCID: https://orcid.org/0000-0001-8338-1168)
- Dapeng Wang (ORCID: https://orcid.org/0000-0002-9925-4574)
- Yue Zhou (ORCID: https://orcid.org/0000-0003-2595-0929)
- Yu‐Ye Li (ORCID: https://orcid.org/0000-0003-0676-985X)
- Hongli Lin (ORCID: https://orcid.org/0000-0001-7229-9855)
- Zhenzhen Yan (ORCID: https://orcid.org/0000-0001-7953-1928)
- Qing Guan
- Qingzhi Wen
Institutions
- Dalian Medical University (CN)
Publication Details
- Journal
- Frontiers in Medicine
- Published
- 2025-12-19
- DOI
- https://doi.org/10.3389/fmed.2025.1704873
- Primary Topic
- Cancer, Hypoxia, and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 0.00