Mechanisms of Chinese Dragon’s Blood on alleviating colonic mucosal damage in mice with ulceratice colitis based on network pharmacology
10.7501/j.issn.0253-2670.2019.16.020
- VernacularTitle: 基于网络药理学分析龙血竭缓解实验性溃疡性结肠炎小鼠结肠黏膜损伤的作用机制
- Author:
Xiao-Juan CUI
1
Author Information
1. Guangxi University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Action mechanism;
Dragon’s blood;
DSS;
Network pharmacology;
Ulcerative colitis
- From:
Chinese Traditional and Herbal Drugs
2019;50(16):3872-3879
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of Chinese Dragon’s Blood (CDB) on DSS-induced ulcerative colitis (UC) in mice, and predict the potential main active ingredients, targets and signaling pathways of CDB by network pharmacology. Methods: Mouse UC model was induced by DSS. Balb/c mice were randomly divided into control group, UC group, CDB high, medium, and low dose group, mesalazine control group, 10 mice in each group. Except the control group, each group drank 3.0% DSS solution freely for seven consecutive days. The CDB group and mesalazine group were given corresponding medicines for gastric perfusion during the modeling period. The mice were weighed regularly every day to conduct occult blood test and observe the animals. The fecal traits were evaluated by DAI. At the end of the experiment, the mice were sacrificed and HE stained and scored. The “compound-compound target-disease target” network was constructed by online databases such as TCMSP, String, Cytoscape, etc, and the target targets of core compound targets and compounds were extracted, GO and KEGG enrichment analysis was performed on related targets. Treatment of biological processes and mechanisms of action that UC may regulate were analyzed. Results: Compared with the control group, the infiltration of inflammatory cells in the model group was obvious, and a large number of cup cells disappeared, and the degree of lesions spread to the muscle layer or even the whole layer; The cup cells in the CDB group re-grew, the extent of the lesion was limited to the mucosa, and the inflammation was alleviated. Through the network pharmacology, 112 target targets of CDB were screened, and 14 core compound targets such as ABL1, F2, and JAK2 could be applied to 11 disease targets such as ICAM1, IL-6, PTGS2, and MTOR. The GO analysis contained 415 enrichment pathways, including 389 biological processes, nine molecular functions, and 17 cell components. The KEGG database was used to enrich the relevant pathways, and 84 pathways such as PI3K-Akt were screened for UC. Conclusion: CDB can alleviate colonic mucosal injury induced by DSS in UC mice. It may regulate the expression of ABL1, F2, JAK2 and other target proteins through flavonoids, and then indirectly regulate the expression of IL-6, PTGS2 and other disease proteins. The JAK2/STAT3 and PI3K-Akt-mTOR pathways regulate the levels of inflammatory factors, inhibit the inflammatory response, and ultimately alleviate UC colonic mucosal damage.
