Effect and Mechanism of Harmine on Echinococcosis Based on Network Pharmacology

Objective The aim of this research was to explore the effects on echinococcosis harmine, an active ingredient Peganum harmala. Methods gene targets were screened out by use online database. STRING exploited build a protein interaction network model, DAVID carry ontology (GO) and Kyoto Encyclopedia Genes Genomes (KEGG) enrichment analyses, AutoDockTools for molecular docking. All mice randomly divided into 3 groups: model group, normal harmine group. Blood indicators detected histological analysis carried out. NCTC-1469 treated with either or control. Gene expression evaluated Western blot. Results Network pharmacological concluded that 6 (HLA-B, HLA-DQB1, IL-6, tumor necrosis factor [TNF], HLA-A, F3) might act as major in treatment harmine. GO function KEGG pathway analyses showed treat mainly regulating immune response. Molecular docking confirmed docked well interactions reliable. Harmine could regulate content inflammatory factors modulate response mice, but caused liver damage. Pathological histology had great suppressive efficacy against infection. However, would have certain negative effect spleen mice. contents HLA-B, TNF, F3 observably enhanced, while Interleukin-6 reduced mouse tissue cells after treatment. As forecast pharmacology, exerted antiechinococcosis multiple pathways. Finally, Th17/Treg balance Conclusions displayed infection These findings suggest be potential therapeutic agent management targeting specific targets.