Network pharmacology and
JingFangFuZiLiZhong formula
bioinformatics
network pharmacology
ulcerative colitis
Journal
Annals of medicine
ISSN: 1365-2060
Titre abrégé: Ann Med
Pays: England
ID NLM: 8906388
Informations de publication
Date de publication:
12 2022
12 2022
Historique:
entrez:
16
11
2022
pubmed:
17
11
2022
medline:
19
11
2022
Statut:
ppublish
Résumé
Ulcerative colitis (UC), a chronic inflammatory disease, often cause carcinogenesis, disability, and intestinal perforation. The JingFangFuZiLiZhong formula (JFFZLZ) shows a good effect against UC in the clinic. Hence, we aim to investigate the mechanisms between JFFZLZ and UC We obtained active constituents and related targets from public databases. The overlapped genes between JFFZLZ and UC targets were further analysed by enrichment analysis. The active constituents and hub targets were used to construct molecule docking analysis. We finally screened out nine hub targets and their expressions were verified in the Gene Expression Omnibus database and UC rats' colon tissues after JFFZLZ treatment. The results implied that JFFZLZ mainly regulated signal transduction, metabolites production, and inflammation pathways. The expression of STAT3, CXCL8, IL6, CXCL12, TNF, TP53, and PTPN11 were both upregulated in colon tissues of UC patients and UC rats. While RELA, EGFR, and TP53 were downregulated in UC patients, but upregulated in UC rats. Furthermore, JFFZLZ could repair UC rats' colon mucosal damage and promote the healing of ulcers These results elucidated that the anti-UC effect of JFFZLZ was closely related to the inhibition of inflammatory response, inhibition of oxidative stress, and repairing colon mucosal damage through different signal pathways. The findings could contribute to a better understanding of the regulation mechanisms in JFFZLZ against UC.Key messagesJFFZLZ could reduce the inflammatory infiltration and repair UC rats' colon mucosal damage.Through the network pharmacology-based strategy and public database mining, we obtained the hub targets and key pathways between JFFZLF and UC.The mechanism of JFFZLZ against UC was inhibition of inflammatory response and oxidative stress by regulating the expression of the hub targets.
Sections du résumé
BACKGROUND
Ulcerative colitis (UC), a chronic inflammatory disease, often cause carcinogenesis, disability, and intestinal perforation. The JingFangFuZiLiZhong formula (JFFZLZ) shows a good effect against UC in the clinic. Hence, we aim to investigate the mechanisms between JFFZLZ and UC
METHODS
We obtained active constituents and related targets from public databases. The overlapped genes between JFFZLZ and UC targets were further analysed by enrichment analysis. The active constituents and hub targets were used to construct molecule docking analysis. We finally screened out nine hub targets and their expressions were verified in the Gene Expression Omnibus database and UC rats' colon tissues after JFFZLZ treatment.
RESULTS
The results implied that JFFZLZ mainly regulated signal transduction, metabolites production, and inflammation pathways. The expression of STAT3, CXCL8, IL6, CXCL12, TNF, TP53, and PTPN11 were both upregulated in colon tissues of UC patients and UC rats. While RELA, EGFR, and TP53 were downregulated in UC patients, but upregulated in UC rats. Furthermore, JFFZLZ could repair UC rats' colon mucosal damage and promote the healing of ulcers
CONCLUSION
These results elucidated that the anti-UC effect of JFFZLZ was closely related to the inhibition of inflammatory response, inhibition of oxidative stress, and repairing colon mucosal damage through different signal pathways. The findings could contribute to a better understanding of the regulation mechanisms in JFFZLZ against UC.Key messagesJFFZLZ could reduce the inflammatory infiltration and repair UC rats' colon mucosal damage.Through the network pharmacology-based strategy and public database mining, we obtained the hub targets and key pathways between JFFZLF and UC.The mechanism of JFFZLZ against UC was inhibition of inflammatory response and oxidative stress by regulating the expression of the hub targets.
Identifiants
pubmed: 36382627
doi: 10.1080/07853890.2022.2095665
pmc: PMC9673803
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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