Mechanism of Modified Danggui Shaoyao San in treatment of chronic atrophic gastritis based on network pharmacology and experimental verification
- Author:
Xiao-Meng LIU
1
;
Yu-Jing MA
1
;
Long-Hui LIU
1
;
Meng-Meng ZHAO
1
;
Zi-Wei DONG
1
;
Qian YANG
2
;
Xiao-Meng LANG
2
;
Yuan ZHAO
2
;
Jian-Ping LIU
2
;
Qian YANG
3
;
Xiao-Meng LANG
3
;
Yuan ZHAO
3
;
Jian-Ping LIU
3
Author Information
- Publication Type:Journal Article
- Keywords: chronic atrophic gastritis; experimetal verification; JAK2/STAT3 signaling pathway; Modified Danggui Shaoyao San; molecular docking; network pharmacology
- From: Chinese Pharmacological Bulletin 2023;39(3):560-568
- CountryChina
- Language:Chinese
- Abstract: Aim To predict the targets of Modified Danggui Shaoyao San ( MDSS) in the treatment of chronic atrophic gastritis ( CAG) based on network pharmacology and vertify the results based on experim-ention. Methods TCMSP, SWISS TARGETS, GENE CARDS and OMIM databases were used to screen the therapeutic targets of MDSS for CAG. STRING database and Cytoscape software were used to construct the protein interaction network and screen the core targets. Metascape database was used for GO analysis and KEGG enrichment pathways. And molecular docking was used for target validation. CAG rat model was pre¬pared by N-methyl-N'-nitroso-N-nitroguanidine free drink combined with sodium salicylate gastric lavage. The pathology of rat gastric mucosa was observed by hematoxylin-eosin staining,and the ultrastructure of ep¬ithelial cells was observed by transmission electron mi-croscopy. The serum IL-6 and IL-10 content was detected by enzyme-linked immunosorbent assay, and the expression of JAK2, STAT3 , p-STAT3 , c-MYC mRNA and protein in rats was detected by qPCR and Western blot. Results MDSS acted on 189 targets, mainly involved in response to oxidative stress and apoptotic signaling pathway. KEGG analysis related to pathways in cancer and JAK-STAT signaling pathway. The experimental results showed that the MDSS could improve the degree of atrophy of gastric mucosa in CAG rats and improve the status of epithelial cells, down-regulate the serum IL-6 content of CAG rats, up-regulate the IL-10 content, and reduce the expression of JAK2, STAT3 , p-STAT3 , c-MYC mRNA and protein in gastric mucosa with statistical significance. Conclusions MDSS treats CAG through multiple active ingredients, targets, and pathways, the mechanism of which may be related to the inhibition of the JAK2/STAT3 signaling pathway.
