AUTHOR=Liao Fei , Yousif Muhammad , Huang Ruya , Qiao Yanlong , Hu Yanchun 

TITLE=Network pharmacology- and molecular docking-based analyses of the antihypertensive mechanism of Ilex kudingcha

JOURNAL=Frontiers in Endocrinology

VOLUME=14

YEAR=2023

URL=https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1216086

DOI=10.3389/fendo.2023.1216086

ISSN=1664-2392

ABSTRACT=<p>Herein, network pharmacology was used to identify the active components in <italic>Ilex kudingcha</italic> and common hypertension-related targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted, and molecular docking was performed to verify molecular dynamic simulations. Six active components in <italic>Ilex kudingcha</italic> were identified; furthermore, 123 target genes common to hypertension were identified. Topological analysis revealed the strongly associated proteins, with <italic>RELA</italic>, <italic>AKT1</italic>, <italic>JUN</italic>, <italic>TP53</italic>, <italic>TNF</italic>, and <italic>MAPK1</italic> being the predicted targets of the studied traditional Chinese medicine. In addition, GO enrichment analysis revealed significant enrichment of biological processes such as oxidative stress, epithelial cell proliferation, cellular response to chemical stress, response to xenobiotic stimulus, and wound healing. Furthermore, KEGG enrichment analysis revealed that the genes were particularly enriched in lipid and atherosclerosis, fluid shear stress and atherosclerosis, and other pathways. Molecular docking revealed that the key components in <italic>Ilex kudingcha</italic> exhibited good binding potential to the target genes <italic>RELA</italic>, <italic>AKT1</italic>, <italic>JUN</italic>, <italic>TP53</italic>, <italic>TNF</italic>, and <italic>IL-6</italic>. Our study results suggest that <italic>Ilex kudingcha</italic> plays a role in hypertension treatment by exerting hypolipidemic, anti-inflammatory, and antioxidant effects and inhibiting the transcription of atherosclerosis-related genes.</p>