Network pharmacology-guided identification of kinase-mediated vascular signalling targets underlying the antihypertensive potential of Brassica rapa L.

Hypertension is a complex cardiometabolic disorder involving oxidative stress, endothelial dysfunction, inflammation, and neurohormonal imbalance, which increases vascular resistance and remodeling. Consequently, single-target treatment frequently has low long-term efficacy. Brassica rapa L. (BRL) turnip, a medicinal and dietary crucifer rich in glucosinolates, flavonoids, and phenolic acids, offers significant potential for blood pressure modulation. Using a comprehensive in silico approach that combines network pharmacology, molecular docking, molecular dynamics simulation, and ADMET-guided screening, this study examines the multitarget antihypertensive potential of BRL. In the list of 189 phytoconstituents identified from extensive databases, 9 drug-like candidates were ultimately selected using SwissADME profiling and Lipinski's rule of 5. Predicted protein targets identified through SwissTargetPrediction and the similarity ensemble approach were cross-referenced with hypertension-associated genes from GeneCards and online Mendelian Inheritance in Man, yielding 246 common targets. Protein-protein interaction analysis identified an essential component comprising 10 hub genes, including EGFR, PIK3CA, FYN, PTK2, SRC, PTPN11, PIK3R1, CTNNB1, and AKT1, indicating a critical role for kinase-driven vascular signalling. The functional enrichment analysis identified redox homeostasis, vascular regulatory balance, and the PI3K-AKT and nitric/eNOS signalling pathways. AutoDock Vina docking identified quercetin (- 11.4 kcal/mol), kaempferol and isorhamnetin (- 11.2 kcal/mol), gluconasturtiin (- 11.2 kcal/mol) as top ligands. Schrodinger molecular dynamics simulations over 100 ns confirmed the stability and energetically favorable nature of the protein-ligand interactions. Overall, BRL demonstrates strong multitarget antihypertensive potential, with prioritized lead molecules for further validation. The online version contains supplementary material available at 10.1007/s40203-026-00671-y.