Exploring the mechanism of Yuchang granule on ulcerative colitis based on network pharmacology and molecular docking
10.12206/j.issn.2097-2024.202407027
- VernacularTitle:基于网络药理学及分子对接研究愈肠颗粒治疗溃疡性结肠炎的分子机制
- Author:
Miao HE
1
;
Can XU
2
;
Shunli LYU
2
;
Jingxia CHEN
1
;
Jing TIAN
3
Author Information
1. Department of Pharmacy, First Affiliated Hospital of Naval Medical University, Shanghai 200433, China.
2. Department of Gastroenterology, The First Affiliated Hospital of Naval Medical University, Shanghai 200433, China.
3. Department of Pharmacy, Naval Medical Center of PLA, Naval Medical University, Shanghai 200052, China.
- Publication Type:Originalarticles
- Keywords:
Yuchang granules;
ulcerative colitis;
network pharmacology;
molecular docking;
mechanisms
- From:
Journal of Pharmaceutical Practice and Service
2026;44(4):209-215
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the molecular mechanism of Yuchang granule (YCG) against ulcerative colitis （UC） by network pharmacology-based approach combined with molecular docking. Methods TCMSP and HIT database were utilized to search the active components and potential targets of YCG. The effective targets of UC were obtained by GeneCards, CTD, and DisGeNET databases. Venn Diagram was exploited to receive common targets of YCG and UC. Network maps of the TCM of YCG-active component-common targets were constructed by the Cytoscape software to gain key active components. Protein-protein interaction （PPI） of common targets was constructed by the STRING database obtaining core common targets. The mechanism and therapeutic effects of YCG on UC were explored via gene ontology （GO） and the biological pathway （KEGG） enrichment analyses. Molecular docking technology was carried out to verify the combination of core active components with key common targets. Results 98 active components and 237 potential targets were sieved from YCG, and 1061 effective targets were screened from UC. 94 common targets of YCG and UC were regarded as potential therapeutic targets. Bioinformatics analysis revealed that quercetin, luteolin, β-quebrachol, stigmasterol, and kaempferol may be the potential candidate agents. Tumor necrosis factor （TNF）, serine/threonine-protein kinase （AKT1）, tumor protein p53 （TP53）, interleukin-6 （IL-6） and IL-1β could become potential therapeutic targets. KEGG showed pathways in cancer, AGE-RAGE signaling pathway in diabetic complications, TNF signaling pathway, and IL-17 signaling pathway might play an important role in YCG against UC. Molecular docking results showed that quercetin combined well with TNF, AKT1, and TP53. And stigmasterol did well with AKT1. Conclusion This study comprehensively illustrated the potential candidate agents, potential therapeutic targets, and pathways of YCG against UC. It also illustrated that YCG could act on multiple targets through multi-pathway treating UC.
