Mechanism of amygdalin for gastric cancer based on network pharmacology and molecular docking
Objective To determine the biological activity,key targets,and potential pharmacological mechanism of amygdalin for gastric cancer based on network pharmacology,molecular docking and in vitro experiments.Methods The relevant targets of amygdalin and gastric cancer were identified and standardized based on data from public databases.The gastric cancer-amygdalin-target network was established with Cytoscape software.Key targets were uploaded to the STRING database for protein-protein interaction(PPI)analysis.Topological analysis identified the core targets of amygdalin therapy in gastric cancer,followed by Gene Ontology and pathway enrichment analyses of Kyoto Encyclopedia of Genes and Genomes enrichment.Molecular docking was used to evaluate the binding affinities between amygdalin and the core targets.In vitro experiments validated these findings,and assessed the therapeutic potential of amygdalin against gastric cancer.Results The CCK-8 results indicated that the proliferation of HGC-27 cells was much inhibited after 48 h of intervention with 4 mg·mL-1 and 8 mg·mL-1 of amygdalin,as compared with the control group.Totally 34 intersecting target genes of amygdalinfor gastric cancer were identified,with the core targets being SSTR1,SSTR2,SSTR3,SSTR4,and SSTR5.Molecular docking analysis showed good binding activity between amygdalin and the 5 core targets.Compared with the control group,the expression levels of Bax and SSTR3 proteins treatly increased,while the expression level of Bc12 protein decreased after 48 h of intervention with 4 mg·mL-1 and 8 mg·mL-1 of amygdalin.Conclusion Amygdalin has a therapeutic effect on gastric cancer by acting as a growth inhibitor on the SSTR3 receptor,increasing the apoptosis of gastric cancer cells,and affecting their growth and proliferation processes.
NETL
NSTL
万方数据
