Complications due to influenza are often associated with inflammation with excessive\nrelease of cytokines. The bulbs of Fritillariae thunbergii (FT) have been traditionally used to\ncontrol airway inflammatory diseases, such as bronchitis and pneumonia. To elucidate active\ncompounds, the targets, and underlying mechanisms of FT for the treatment of influenza-induced\ninflammation, systems biology was employed. Active compounds of FT were identified through\nthe TCMSP database according to oral bioavailability (OB) and drug-likeness (DL) criteria.\nOther pharmacokinetic parameters, Caco-2 permeability (Caco-2), and drug half-life (HL) were\nalso identified. Biological targets of FT were retrieved from DrugBank and STITCH databases,\nand target genes associated with influenza, lung, and spleen inflammation were collected from\nDisGeNET and NCBI databases. Compound-disease-target (C-D-T) networks were constructed and\nmerged using Cytoscape. Target genes retrieved from the C-D-T network were further analyzed with\nGO enrichment and KEGG pathway analysis. In our network, GO and KEGG results yielded two\ncompounds (beta-sitosterol (BS) and pelargonidin (PG)), targets (PTGS1 (COX-1) and PTGS2 (COX-2)),\nand pathways (nitric oxide, TNF) were involved in the inhibitory effects of FT on influenza-associated\ninflammation. We retrieved the binding affnity of each ligand-target, and found that PG and COX-1\nshowed the strongest binding affnity among four binding results using a molecular docking method.\nWe identified the potential compounds and targets of FT against influenza and suggest that FT is an\nimmunomodulatory therapy for influenza-associated inflammation.
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