Objective The study aimed to explore the mechanism of Mume Fructus and Rosa multiflora in the treatment of recurrent oral ulceration(ROU)through network pharmacology and animal experiments.Methods The chemical components of Mume Fructus and Rosa multiflora were filtrated by OB and DL,which were respectively searched from TCMSP and references.The targets were predicted by TCMSP and Swiss Target Prediction.The targets of ROU were searched from OMIM and GeneCards database.Cystoscape 3.2.1 software was used to construct the"components-targets"network and analysis gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway with Clue GO.The protein-protein interaction(PPI)network analysis was carried out on the common targets by String database and Cystoscape 3.2.1 software.Moreover,after constructing the rat model of ROU,the pathological changes of oral mucosa of rats were observed by HE staining,and the effects of Mume Fructus and Rosa multiflora on inflammatory factors and key targets were detected by ELISA and Western blot.Results 33 active ingredients were selected for treating ROU,among which quercetin,ursolic acid,β-sitosterol,stigmasterol,palmitic acid,apioline and kaempferol were the core components.Key targets such as STAT3,PIK3R1,PIK3CA,STAT1,JAK2 and IL-6 were screened.GO functional enrichment and KEGG enrichment analysis showed that the core targets mainly affected the process of response to organic substance,cellular response to chemical stimulus and cellular response to organic substance,involving NF-κB,JAK-STAT,IL-17 and other signaling pathways.Experimental results in rats showed that Mume Fructus and Rosa multiflora could significantly improve the pathological status of ulcer mucosal tissue,reduce the expression of IL-1β,IL-6,TNF-α and IFN-γ,and reduce the expression of JAK2 and STAT1 in oral mucosa.Conclusion The anti-ROU effect of Mume Fructus and Rosa multiflora may be achieved by regulating the JAK2-STAT1 signaling pathway,reducing the levels of IL-1β,IL-6,TNF-α and IFN-γ inflammatory factors.

Objective The study aimed to explore the mechanism of Mume Fructus and Rosa multiflora in the treatment of recurrent oral ulceration(ROU)through network pharmacology and animal experiments.Methods The chemical components of Mume Fructus and Rosa multiflora were filtrated by OB and DL,which were respectively searched from TCMSP and references.The targets were predicted by TCMSP and Swiss Target Prediction.The targets of ROU were searched from OMIM and GeneCards database.Cystoscape 3.2.1 software was used to construct the"components-targets"network and analysis gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway with Clue GO.The protein-protein interaction(PPI)network analysis was carried out on the common targets by String database and Cystoscape 3.2.1 software.Moreover,after constructing the rat model of ROU,the pathological changes of oral mucosa of rats were observed by HE staining,and the effects of Mume Fructus and Rosa multiflora on inflammatory factors and key targets were detected by ELISA and Western blot.Results 33 active ingredients were selected for treating ROU,among which quercetin,ursolic acid,β-sitosterol,stigmasterol,palmitic acid,apioline and kaempferol were the core components.Key targets such as STAT3,PIK3R1,PIK3CA,STAT1,JAK2 and IL-6 were screened.GO functional enrichment and KEGG enrichment analysis showed that the core targets mainly affected the process of response to organic substance,cellular response to chemical stimulus and cellular response to organic substance,involving NF-κB,JAK-STAT,IL-17 and other signaling pathways.Experimental results in rats showed that Mume Fructus and Rosa multiflora could significantly improve the pathological status of ulcer mucosal tissue,reduce the expression of IL-1β,IL-6,TNF-α and IFN-γ,and reduce the expression of JAK2 and STAT1 in oral mucosa.Conclusion The anti-ROU effect of Mume Fructus and Rosa multiflora may be achieved by regulating the JAK2-STAT1 signaling pathway,reducing the levels of IL-1β,IL-6,TNF-α and IFN-γ inflammatory factors.