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Mechanism of Epigallocatechin-3-gallate in the prevention and treatment of irritable bowel syndrome: A network pharmacology and gene expression omnibus chip data-based study
被引:0
|作者:
Ye, Fangchen
[1
,2
]
Li, Laifu
[1
,2
]
Wang, Lianli
[1
,2
]
Ran, Yan
[1
,2
]
Mei, Lin
[1
,2
]
Sun, Yating
[1
,2
]
Zhang, Xinping
[1
,2
]
Dai, Fei
[1
,2
]
机构:
[1] Xi An Jiao Tong Univ, Dept Gastroenterol, Affiliated Hosp 2, Xian, Peoples R China
[2] Xi An Jiao Tong Univ, Shaanxi Prov Key Lab Gastrointestinal Motil Disord, Lab Digest Dis, Affiliated Hosp 2, Xian, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
Irritable bowel syndrome;
Green tea;
Network pharmacology;
Pharmacological mechanism;
GREEN TEA;
MICROBIOTA;
DISORDERS;
CYTOKINES;
D O I:
10.1016/j.phanu.2025.100433
中图分类号:
R914 [药物化学];
学科分类号:
100701 ;
摘要:
Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder, characterized by abdominal pain, bloating, and changes in bowel habits. Green tea has been reported to possess anti-inflammatory and antioxidant properties, which may aid in improving intestinal inflammation. However, the targets and mechanisms of green tea in treating IBS are still unclear. In this study, we utilized network pharmacology and molecular docking techniques in combination with Gene Expression Omnibus (GEO) chip analysis and bioinformatics analysis. Our aim was to explore the molecular targets and mechanisms of Epigallocatechin-3-gallate (EGCG), the primary active component found in green tea, for the prevention and treatment of IBS. We obtained 164 drug targets, 335 differentially expressed genes of IBS, and 12 drug-disease cross genes. After screening the results, TNF, TLR4, PTGS2, and IL10 were identified as core targets. Molecular docking results confirmed that EGCG binds to these core targets and can be used for the prevention and treatment of IBS. Then, we stimulated M1-type macrophages with EGCG and showed that EGCG up-regulated mRNA of IL10 and down-regulated mRNA of TNF and TLR4 in macrophages. This study suggests that EGCG may be involved in inflammation-related signaling pathways and plays a key role in the prevention and treatment of IBS by acting on disease targets such as TNF, TLR4, PTGS2, and IL10.
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