{"title":"Exploring the Modern Pharmacological Mechanism of Special Ingredients of Panax Ginseng for Ulcerative Colitis based on Network Pharmacology","authors":"Weichen Si","doi":"10.14218/fim.2022.00058","DOIUrl":null,"url":null,"abstract":"Background and Objective: To explore the main action targets and key pathways, along with their mechanisms of action, of Panax ginseng’s special ingredients in the treatment of ulcerative colitis using network pharmacology methods. To provide a theoretical basis for subsequent laboratory experiments and clinical trials. Methods: The main active ingredients of Panax notoginseng were obtained through the TCMSP database and the specific ingredients were screened. The targets of Panax notoginseng-specific components were obtained from the Swiss Target Prediction database. The GeneCards, OMIM, and DisGent databases were used to obtain the targets related to ulcerative colitis. The protein interaction network (PPI) of intersecting targets was constructed using the STRING database. GO function and KEGG pathway enrichment analysis were performed in R language software. Construction of the herb-component-target-disease-KEGG pathway network was achieved using Cytoscape software. Results: Seven major active ingredients of Panax notoginseng were obtained, and ginsenoside f2 was found to be a special ingredient, corresponding to 16 potential targets. A search of the disease database yielded 5,536 targets for ulcerative colitis. Eight core targets were obtained by protein interaction analysis of the intersecting targets: STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, BCL2L1, and RORC, respectively. 417 entries were obtained by GO functional enrichment analysis, and 22 statistically significant pathways were obtained by KEGG enrichment analysis. Conclusion: The mechanism of action of ginsenoside f2 in the treatment of ulcerative colitis features multi-target and multi-pathway interactions. The receptors may be related to STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, and other targets, and the main signaling pathways may be related to the PI3K-Akt signaling pathway, Th17 cell differentiation, and inflammatory bowel disease among others and this provides a theoretical basis for the next in-depth experimental study.","PeriodicalId":73126,"journal":{"name":"Future integrative medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Future integrative medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14218/fim.2022.00058","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background and Objective: To explore the main action targets and key pathways, along with their mechanisms of action, of Panax ginseng’s special ingredients in the treatment of ulcerative colitis using network pharmacology methods. To provide a theoretical basis for subsequent laboratory experiments and clinical trials. Methods: The main active ingredients of Panax notoginseng were obtained through the TCMSP database and the specific ingredients were screened. The targets of Panax notoginseng-specific components were obtained from the Swiss Target Prediction database. The GeneCards, OMIM, and DisGent databases were used to obtain the targets related to ulcerative colitis. The protein interaction network (PPI) of intersecting targets was constructed using the STRING database. GO function and KEGG pathway enrichment analysis were performed in R language software. Construction of the herb-component-target-disease-KEGG pathway network was achieved using Cytoscape software. Results: Seven major active ingredients of Panax notoginseng were obtained, and ginsenoside f2 was found to be a special ingredient, corresponding to 16 potential targets. A search of the disease database yielded 5,536 targets for ulcerative colitis. Eight core targets were obtained by protein interaction analysis of the intersecting targets: STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, BCL2L1, and RORC, respectively. 417 entries were obtained by GO functional enrichment analysis, and 22 statistically significant pathways were obtained by KEGG enrichment analysis. Conclusion: The mechanism of action of ginsenoside f2 in the treatment of ulcerative colitis features multi-target and multi-pathway interactions. The receptors may be related to STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, and other targets, and the main signaling pathways may be related to the PI3K-Akt signaling pathway, Th17 cell differentiation, and inflammatory bowel disease among others and this provides a theoretical basis for the next in-depth experimental study.