Research Paper Volume 16, Issue 2 pp 1911—1924
Investigation of Tongxie-Yaofang formula in treating ulcerative colitis based on network pharmacology via regulating MAPK/AKT signaling pathway
- 1 Department of Proctology, Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang 330000, China
- 2 Formula-Pattern Research Center of Traditional Chinese Medicine, Nanchang 330000, China
Received: September 18, 2023 Accepted: December 4, 2023 Published: January 24, 2024
https://doi.org/10.18632/aging.205467How to Cite
Copyright: © 2024 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: Ulcerative colitis (UC) is a subtype of inflammatory bowel disease, which often leads to bloody diarrhea and abdominal pain. In this study, the function mechanism of Tongxie-Yaofang formula (TXYF) on UC was investigated.
Methods: Action targets of TXYF were obtained by Traditional Chinese Medicine Systems Pharmacology Database (TCMSP) and Traditional Chinese Medicine Integrated Database (TCMID) databases. The targets of UC were screened in Gene Cards and Online Mendelian Inheritance in Man (OMIM) databases. The network pharmacology of active ingredient targets was established via Cytoscape.
Results: A total of 42 chemical components and 5806 disease targets were obtained. The GO functional analysis showed that biological processes such as oxidative stress and molecular response to bacteria, molecular function such as protein and nucleic acid binding activity were significantly enriched. The top 20 KEGG enriched signal pathways indicated that the targets were mainly linked with IL-17, TNF, HIF-1. Molecular docking results showed that naringenin had good binding activity between naringin and MAPK, albiflorin and SRC. The activity of MPO, the concentration of HIF-1, IL-17 and TNF-α were significantly decreased after TXYF treatment. The characteristics of UC such as crypt distortion, crypt atrophy, and increased basal plasmacytosis were also less observed with the treatment of TXYF. What’s more, TXYF suppresses the phosphorylation of SRC, MAPK and AKT1 in UC.
Conclusions: TXYF showed treatment effect on UC through multiple components and multiple targets, which lays a foundation for further study of UC treatment.