The mechanism of quercetin in treating intracerebral hemorrhage was investigated by network pharmacology and molecular docking.

Background: The aim of this study was to explore the molecular mechanism of quercetin in the treatment of intracerebral hemorrhage.
Methods: Quercetin target genes and intracerebral hemorrhage target genes were collected from 5 databases. After standardized conversion of the obtained target genes through uniprot database, cross genes of the 2 were obtained using Venny 2.1 online tool. Further, protein interaction relationships were obtained in the String database, and then core target genes were screened and visualized by Cytoscape software, and cross genes were enriched by GO and KEGG pathways. Finally, the active drug ingredients and target proteins were verified and visualized by computer.
Results: In this study, 197 quercetin targets were identified as potential targets for the treatment of intracerebral hemorrhage, and 7 core target genes (TP53, STAT3, AKT1, SRC, JUN, TNF, and IL6) were screened. The GO and KEGG analyses further shed light on the molecular mechanisms underlying quercetin's treatment of intracerebral hemorrhage, involving multiple biological processes and signaling pathways (such as cancer pathways, lipids, and atherosclerosis). The stable binding of quercetin to these 7 key targets was confirmed by molecular docking simulation.
Conclusion: Quercetin may treat intracerebral hemorrhage through multi-target-multi-pathway mechanisms, including regulating apoptosis, inhibiting inflammatory response, inhibiting iron death, and regulating angiogenesis, which can help alleviate nerve damage caused by intracerebral hemorrhage.
Competing Interests: The authors have no conflicts of interest to disclose.
(Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)