Mechanism of Shaoyaotang in Treatment of Ulcerative Colitis Based on Network Pharmacology and Experimental Verification
10.13422/j.cnki.syfjx.20230822
- VernacularTitle:基于网络药理学及实验验证探讨芍药汤治疗溃疡性结肠炎的作用机制
- Author:
Yini LI
1
;
Yunan ZHANG
1
;
Lu ZHAO
1
;
Lulu WANG
2
;
Yali ZHOU
1
;
Jianhua ZHEN
1
Author Information
1. School of Life Sciences， Beijing University of Chinese Medicine， Beijing 100029，China
2. Dongzhimen Hospital， Beijing University of Chinese Medicine， Beijing 100029，China
- Publication Type:Journal Article
- Keywords:
Shaoyaotang;
ulcerative colitis;
network pharmacology;
animal experiment;
5-hydroxytryptamine （5-HT）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(23):8-15
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the mechanism of Shaoyaotang （SYT） in the treatment of ulcerative colitis （UC） based on network pharmacology and experimental verification. MethodThe core components， target genes， and main pathways of SYT were predicted based on network pharmacology， and UC-related components， target genes， and pathways were screened. Dextran sodium sulfate （DSS） was used to induce the UC model in mice， and the effect of SYT on UC mice was observed， followed by mechanism verification. ResultNetwork pharmacology indicated that 174 active components and corresponding 159 target genes of SYT were screened， and the related pathways were those mediated by 5-hydroxytryptamine （5-HT） degredation and 5-HT receptor 3. The results of animal experiments showed that compared with the model group， the SYT group showed increased body weight and colon length（P<0.01）， reduced disease activity index （DAI） score （P<0.01）， improved histopathological manifestations， reduced concentrations of 5-HT in the colonic tissues and serum （P<0.05， P<0.01）， and increased mRNA expression of monoamine oxidase A （MAOA）， monoamine oxidase B （MAOB）， sodium-dependent serotonin transporter （SLC6A4）， and 5-HT receptor 3A （5-HTR3A） related to 5-HT metabolism in the colon （P<0.01）. ConclusionSYT can alleviate the local inflammatory response of the intestinal tract in UC by regulating 5-HT degredation pathways.
