Mechanism of Trigonella foenum-graecum L.in Regulating Ferroptosis for Treatment of Traumatic Brain Injury
Objective:This study aims to explore the mechanism of Trigonella foenum-graecum L.in regulating ferroptosis for the treatment of traumatic brain injury(TBI)through network pharmacology and molecular docking techniques.Methods:The major active components and target genes of Trigonella foenum-graecum L.were obtained from the TCMSP and PubChem databases.TBI-related genes and ferroptosis-related genes were screened using the GeneCards and OMIM databases.The common targets of the three sets of genes were identified using the Venny 2.1.0 online platform to recognize potential thera-peutic targets.The"Trigonella foenum-graecum L.-Active Ingredients-Targets"network was constructed using Cytoscape software,and a protein-protein interaction(PPI)network was generated using the STRING database.Subsequently,gene ontology(GO)functional enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis were performed using Metascape.Finally,molecular docking analysis was carried out using maestro software.Results:Eleven active components of Trigonella foenum-graecum L.and 285 targets were identified,with 2 189 TBI-related targets,1 407 ferroptosis-related targets,and 29 common targets among the three.The PPI network revealed that MTOR,HSP90AA1,JUN and AKT1 were the key targets.KEGG pathway analysis indicated that Trigonella foenum-graecum L.may improve TBI through the PI3K/Akt and MAPK signaling pathways.Molecular docking results demonstrated that Trigonelline(the key active ingredient of Trigonella foenum-graecum L.)showed favorable binding with MTOR,HSP90AA1,JUN and AKT1.Conclusion:Trigonella foenum-graecum L.and its active component,Trigonelline,may regulate ferroptosis and treat TBI by modulating the PI3K/Akt and MAPK pathways,affecting genes such as MTOR and AKT1.
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