Potential mechanism of vitexin in ameliorating myocardial ischemia reperfusion injury by ferroptosis based on network pharmacology
Objective To study the molecular mechanism of vitexin in improving myocardial ischemia reperfusion injury through iron death pathway based on the biological information database platform,network pharmacology,and molecular docking techniques.Methods To screen potential targets of vitexin and related targets of myocardial ischemia reperfusion injury by multiple databases.After intersection,PPI network was constructed and core targets were screened.GO function and KEGG pathway enrichment analysis were performed on the intersection targets.Construct the"vitexin-target-pathway"network and screen the key core targets and pathways.Further,the intersection of potential targets of vitexin,iron death-related targets,and myocardial ischemia reperfusion injury related targets was selected,and the key core targets related to vitexin,iron death-myocardial ischemia reperfusion injury were screened.Molecular docking was used to study the binding mechanism between vitexin and key core targets.Results A total of 74 intersecting targets of vitexin and myocardial ischemia reperfusion injury were screened out.Among which,22 core targets including tumor necrosis factor(TNF),lymphoblastoma-2(Bcl-2)and estrogen receptor 1(ESR1)were identified,these core targets participate extensively in signaling pathways related to lipid metabolism,atherosclerosis,and the IL-17 pathway.Molecular docking results indicated that vitexin could bind to the tested key targets through hydrogen bonds,van der Waals forces,π-π interactions,and other interactions.Conclusion Vitexin can ameliorate myocardial ischemiation reperfusion injury by inhibiting inflammatory response,apoptosis,regulating iron homeostasis and limiting iron death through oxidative stress.
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