Exploring the mechanism of Portulaca oleracea inhibiting inflammatory response in pigs based on network pharmacology and molecular docking techniques
Using such technologies as network pharmacology and molecular docking,the study explored the main active components and key targets of portulaca oleracea in inhibiting pig inflammatory response,and investigated its mechanism of action.Traditional Chinese Medicine System Pharmacology Database and Analysis Platform and Uniprot(Universal Protein)were used to screen the active components of portulaca oleracea and their action targets.The GeneCards and Therapeutic Target Database were used to obtain inflammation-related targets.Using the website of Venn,the study constructed a Venn diagram by mapping portulaca oleracea-related targets and inflammation-related targets,obtaining the predicted targets of portulaca oleracea inhibiting inflammation in pigs.The predicted targets were further screened by the database of String and the software of Cytoscape.After the key targets were obtained,GO functional enrichment analysis and KEGG pathway enrichment analysis were carried out,and the top-ranked key targets and active ingredients were finally selected to conduct molecular docking studies.The results show that a total of 10 potential pharmacological components,such as β-sitosterol,kaempferol and lignans,are obtained.portulaca oleracea exerts anti-inflammatory effects through 90 core targets including TNF,ALB and TP53.These targets participate in many biological processes such as positive regulation of cell migration,inflammatory response,and the response of molecules of bacterial origin,and are involved in the signaling pathways,such as cancer,malaria,and MAPK.This study reveals the mechanism of action of portulaca oleracea as a multi-component,multi-target and multi-pathway inhibitor of porcine inflammatory response,and provides a theoretical basis for its specific mechanism of treating porcine diarrhea-related diseases caused by inflammatory response in actual animal husbandry.