Study on the Anti-inflammatory Effect of Lactiplantibacillus plantarum HCS03-001 Based on Zebrafish Model and Network Pharmacology
Excessive inflammation is seriously harmful to human health.The anti-inflammatory effect of Lactiplantibacillus planta-rum HCS03-001 was verified and the anti-inflammatory mechanism was explored.Using transgenic neutrophil green fluorescent zebrafish as model,bacterial LPS was used to induce inflammation,and indomethacin was used as positive control to explore the anti-bacterial inflammatory effect of Lactiplantibacillus plantarum HCS03-001 of 10,20 and 40 mg·mL-1.The main components and inflammatory targets of the metabolites of Lactiplantibacillus plantarum were obtained by SwissTargetPrediction,GeneCards and DisGeNET database.After the targets were intersected,the PPI network was constructed by STRING database,the metabol-ic product"component-target-inflammation"network was constructed by Cytoscape3.9.0,and the common targets were analyzed by GO enrichment analysis and KEGG pathway enrichment analysis using DAVID platform tools.The results of zebrafish experi-ment showed that different doses of HCS03-001 could reduce the number of neutrophils in zebrafish yolk sac,and the effect of high dose(40 mg·mL-1)was significantly higher than that of the model group.The results of network pharmacology showed that in the process of relieving inflammation,the main active components of Lactobacillus plantarum metabolites were isopyridine thi-amine,indole acetaldehyde and ergothione,which may act on core targets such as GAPDH,Ptgs2 and PPARγ.The enrichment results showed that the most significant biological process was the response to LPS,the cell components involved were cell mem-branes,and the most significant pathway was cancer pathway.The results showed that Lactiplantibacillus plantarum HCS03-001 had a significant anti-bacterial inflammatory effect,and the specific mechanism may be that metabolic components such as iso-pyridine thiamine,indole acetaldehyde and ergothione affect cancer-related pathways by inhibiting the binding of bacterial LPS to the plasma membrane and regulating key targets such as GAPDH,Ptgs2 and PPARγ.
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