Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 14, 2022; 28(34): 5007-5022
Published online Sep 14, 2022. doi: 10.3748/wjg.v28.i34.5007
Ji-Chuan decoction ameliorates slow transit constipation via regulation of intestinal glial cell apoptosis
Xiu-Min Wang, Li-Xia Lv, Yue-Si Qin, Yu-Zhu Zhang, Ni Yang, Shu Wu, Xiu-Wen Xia, Hong Yang, Hong Xu, Ying Liu, Wei-Jun Ding
Xiu-Min Wang, Yu-Zhu Zhang, Ni Yang, Shu Wu, Xiu-Wen Xia, Hong Yang, Wei-Jun Ding, Department of Fundamental Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610072, Sichuan Province, China
Xiu-Min Wang, Hong Xu, Department of Proctology, Chengdu First People’s Hospital, Chengdu 610041, Sichuan Province, China
Li-Xia Lv, Department of Endocrinology and Metabolism, Chengdu First People’s Hospital, Chengdu 610041, Sichuan Province, China
Yue-Si Qin, Department of Dermatology, Chengdu First People’s Hospital, Chengdu 610041, Sichuan Province, China
Ying Liu, Department of Preventive Medicine, Shantou University Medical College, Shantou 515063, Guangdong Province, China
Author contributions: Wang XM, Xu H, and Ding WJ designed and coordinated the study; Wang XM, Lv LX, Qin YS, Zhang YZ, Yang N, Wu S, Xia XW, and Yang H performed the experiments and acquired and analyzed the data; Liu Y interpreted the data; Ding WJ contributed to critical revision of the manuscript; and all authors read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 82074151; and the Experimental Formulary Sichuan Youth Science and Technology Innovation Research Team, No. 2020JDTD0022.
Institutional animal care and use committee statement: This experiment was approved by the Animal Ethics Committee, Chengdu University of TCM (license 2016-16).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Wei-Jun Ding, PhD, Full Professor, Department of Fundamental Medicine, Chengdu University of Traditional Chinese Medicine, No. 1166 Liutai Avenue, Wenjiang District, Chengdu 610072, Sichuan Province, China. dingweijun@cdutcm.edu.cn
Received: May 20, 2022
Peer-review started: May 20, 2022
First decision: July 13, 2022
Revised: July 19, 2022
Accepted: August 21, 2022
Article in press: August 21, 2022
Published online: September 14, 2022
ARTICLE HIGHLIGHTS
Research background

Slow transit constipation (STC) is a common intestinal disorder without an effective therapeutic regimen. Ji-Chuan Decoction (JCD) is an established formula for STC. However, its pharmacological mechanism is still unclear.

Research motivation

To determine the ingredients and mechanism of JCD for STC treatment.

Research objectives

To explore the integrated regulatory pattern of JCD against STC through hyphenated techniques from metabolism, network pharmacology and molecular methods.

Research methods

STC model mice were generated by gavage of diphenoxylate for 14 d. STC mice in the low- (3.04 g/kg), medium- (6.08 g/kg) and high-dosage (12.16 g/kg) JCD groups were orally administered. The acetylcholine (ACH) level was detected by enzyme-linked immunosorbent assay. AKT expression and enteric glial cell (EGC) apoptosis were demonstrated by immunofluorescence. The differentially expressed metabolites were tested by nontargeted metabolomics. The targets and core ingredients were identified by network pharmacology.

Research results

JCD significantly promotes intestinal motility, increases colonic ACH content and reduces inflammation in STC mice. It markedly restores the misaligned metabolites, including taurine/hypotaurine, and rescues AKT expression with quercetin. Inhibition of EGC apoptosis is a potential mechanism by which JCD relieves constipation.

Research conclusions

Regulating gut metabolites and reducing EGC apoptosis in STC mice may be the key mechanism of JCD for STC treatment.

Research perspectives

Further investigation into the molecular interactions among the JCD ingredients and metabolites, intestinal microbiota and host response in STC mice is necessary.