Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence

Background: Prunetin (Pru), a bioactive flavonoid present in Caulis spatholobi, has been reported to possess a variety of pharmacological effects. However, the therapeutic effect and underlying mechanisms of Pru in inflammatory bowel disease have not been previously investigated. This study aimed to...

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Main Authors: Ludi Fan, Jinglong Shi, Xiaobo Yang
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:All Life
Subjects:
Online Access:http://dx.doi.org/10.1080/26895293.2022.2164359
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author Ludi Fan
Jinglong Shi
Xiaobo Yang
author_facet Ludi Fan
Jinglong Shi
Xiaobo Yang
author_sort Ludi Fan
collection DOAJ
description Background: Prunetin (Pru), a bioactive flavonoid present in Caulis spatholobi, has been reported to possess a variety of pharmacological effects. However, the therapeutic effect and underlying mechanisms of Pru in inflammatory bowel disease have not been previously investigated. This study aimed to explore the protective action of Pru on dextran sulfate sodium (DSS)-induced colitis by network pharmacology and experimental validation. Methods: The corresponding genes of Pru were predicted using the Comparative Toxicogenomics Database (CTD) and SwissTargetPrediction. Differentially expressed genes (DEGs) between the control rats and DSS-induced colitis rats were identified from the microarray profile GSE54005. Cytoscape software was used to visualize the protein–protein interaction (PPI) networks of overlapped targets. Besides, an animal experiment was performed to verify the therapeutic effect of Pru on colitis. Results: 21 potential targets related to colitis treated by Pru were identified. The topological analysis revealed that Tnf, Il6, and Il1b were the key genes. The KEGG and GO enrichment analyses showed that key targets were enriched in the inflammatory bowel disease, IL-17 signaling pathway, TNF signaling pathway, regulation of inflammatory response, and acute inflammatory response. The in vivo experiment revealed that Pru improves pathological injury and alleviated colitis symptoms via the regulation of Tnf, Il6, and Il1b, which were involved in the acute inflammatory response. Conclusion: Our findings demonstrated that Pru alleviates colitis symptoms through the regulation of inflammatory response, which provides a scientific basis for Pru in preventing and treating colitis.
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spelling doaj.art-ab3eb1f769484e50a8393893b3457c692023-12-07T15:12:04ZengTaylor & Francis GroupAll Life2689-53072023-12-0116110.1080/26895293.2022.21643592164359Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidenceLudi Fan0Jinglong Shi1Xiaobo Yang2Guangzhou University of Chinese MedicineGuangzhou Twelfth People’s HospitalGuangzhou University of Chinese MedicineBackground: Prunetin (Pru), a bioactive flavonoid present in Caulis spatholobi, has been reported to possess a variety of pharmacological effects. However, the therapeutic effect and underlying mechanisms of Pru in inflammatory bowel disease have not been previously investigated. This study aimed to explore the protective action of Pru on dextran sulfate sodium (DSS)-induced colitis by network pharmacology and experimental validation. Methods: The corresponding genes of Pru were predicted using the Comparative Toxicogenomics Database (CTD) and SwissTargetPrediction. Differentially expressed genes (DEGs) between the control rats and DSS-induced colitis rats were identified from the microarray profile GSE54005. Cytoscape software was used to visualize the protein–protein interaction (PPI) networks of overlapped targets. Besides, an animal experiment was performed to verify the therapeutic effect of Pru on colitis. Results: 21 potential targets related to colitis treated by Pru were identified. The topological analysis revealed that Tnf, Il6, and Il1b were the key genes. The KEGG and GO enrichment analyses showed that key targets were enriched in the inflammatory bowel disease, IL-17 signaling pathway, TNF signaling pathway, regulation of inflammatory response, and acute inflammatory response. The in vivo experiment revealed that Pru improves pathological injury and alleviated colitis symptoms via the regulation of Tnf, Il6, and Il1b, which were involved in the acute inflammatory response. Conclusion: Our findings demonstrated that Pru alleviates colitis symptoms through the regulation of inflammatory response, which provides a scientific basis for Pru in preventing and treating colitis.http://dx.doi.org/10.1080/26895293.2022.2164359inflammationbioinformatics analysisil-6prunetincolitis
spellingShingle Ludi Fan
Jinglong Shi
Xiaobo Yang
Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
All Life
inflammation
bioinformatics analysis
il-6
prunetin
colitis
title Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
title_full Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
title_fullStr Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
title_full_unstemmed Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
title_short Prunetin alleviates dextran sulfate sodium-induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
title_sort prunetin alleviates dextran sulfate sodium induced colitis via the regulation of inflammatory response based on network pharmacology and experimental evidence
topic inflammation
bioinformatics analysis
il-6
prunetin
colitis
url http://dx.doi.org/10.1080/26895293.2022.2164359
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AT jinglongshi prunetinalleviatesdextransulfatesodiuminducedcolitisviatheregulationofinflammatoryresponsebasedonnetworkpharmacologyandexperimentalevidence
AT xiaoboyang prunetinalleviatesdextransulfatesodiuminducedcolitisviatheregulationofinflammatoryresponsebasedonnetworkpharmacologyandexperimentalevidence