Exploring the Mechanisms of Resveratrol in <scp>ARDS</scp> Treatment: From Network Pharmacology and Molecular Docking to In Vitro Validation
Acute respiratory distress syndrome (ARDS) is a severe and critical clinical pulmonary disease. Resveratrol (RES), a non-flavonoid polyphenolic compound, has shown potential therapeutic effects. However, the underlying mechanism of RES treatment for ARDS remains unclear. This study employed network pharmacology to predict potential targets and metabolic pathways involved in RES treatment for ARDS. Molecular docking and experimental validation were performed to confirm key targets and metabolic pathways. A comprehensive database search identified 115 RES-ARDS-related targets. Subsequently, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses highlighted the JAK/STAT pathway, which was further investigated with RES in the treatment of ARDS. Hematoxylin-eosin (HE) staining visualized lung damage. Western blot analysis showed that RES significantly downregulated p-JAK2, NLRP3, IL-18, and p-STAT3 expression (p < 0.05). A variety of animal experiments have substantiated that RES can effectively inhibit inflammation and oxidative stress, and promote blood barrier repair. In conclusion, this study provides new insights into the protective mechanism of RES against ARDS, highlighting its potential as a therapeutic agent.
Authors
- Ying Yu (ORCID: https://orcid.org/0000-0003-0925-0148)
- Wei‐Ping Zhang (ORCID: https://orcid.org/0000-0001-5229-5849)
- Xianling Cong (ORCID: https://orcid.org/0000-0002-5790-4188)
- Siyu Sun
- Meng Qin (ORCID: https://orcid.org/0000-0002-5448-2477)
- Junjie Zhang (ORCID: https://orcid.org/0000-0002-7145-8233)
- Wanting Hu (ORCID: https://orcid.org/0009-0009-6267-0273)
- Zhili Zhang
Institutions
- Bengbu Medical College (CN)
Publication Details
- Journal
- Chemical Biology & Drug Design
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1111/cbdd.70187
- Primary Topic
- Cytokine Signaling Pathways and Interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00