Copyright
©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 14, 2022; 28(46): 6522-6536
Published online Dec 14, 2022. doi: 10.3748/wjg.v28.i46.6522
Published online Dec 14, 2022. doi: 10.3748/wjg.v28.i46.6522
3,6-dichlorobenzo[b]thiophene-2-carboxylic acid alleviates ulcerative colitis by suppressing mammalian target of rapamycin complex 1 activation and regulating intestinal microbiota
Qiong-Zi He, Peng Wei, Jun-Zhi Zhang, Tong-Tong Liu, Kun-Qun Shi, Huan-Huan Liu, Shi-Jia Liu, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing 210029, Jiangsu Province, China
Qiong-Zi He, Peng Wei, Jun-Zhi Zhang, Tong-Tong Liu, Kun-Qun Shi, Huan-Huan Liu, College of The First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu Province, China
Jing-Wei Zhang, School of Life Science and Technology, China Pharmaceutical University, Nanjing 211198, Jiangsu Province, China
Author contributions: He QZ and Wei P contributed equally to this work; He QZ, Wei P, and Liu HH conceived and performed experiments; He QZ, Zhang JZ, Liu TT, and Shi KQ analyzed the data; He QZ and Wei P wrote the paper; Liu SJ revised the manuscript and obtained funding for the project; All authors read and approved the final manuscript.
Supported by National Natural Science Foundation of China , No. 82074241 ; and Project of Jiangsu Province Hospital of Traditional Chinese Medicine Peak Talent , No. y2021rc36 .
Institutional animal care and use committee statement: All experimental procedures with mice were performed in accordance and in compliance with the regulations of the Pharmacological Laboratory and Animal Ethics Committee in Affiliated Hospital of Nanjing University of Traditional Chinese Medicine (SYXK2017-0069).
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 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: Shi-Jia Liu, PhD, Research Fellow, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing 210029, Jiangsu Province, China. liushijia2011@163.com
Received: July 20, 2022
Peer-review started: July 20, 2022
First decision: October 22, 2022
Revised: November 4, 2022
Accepted: November 22, 2022
Article in press: November 22, 2022
Published online: December 14, 2022
Processing time: 140 Days and 18.8 Hours
Peer-review started: July 20, 2022
First decision: October 22, 2022
Revised: November 4, 2022
Accepted: November 22, 2022
Article in press: November 22, 2022
Published online: December 14, 2022
Processing time: 140 Days and 18.8 Hours
Core Tip
Core Tip: Gut microbiota dysbiosis and hyperactivated mammalian target of rapamycin complex 1 (mTORC1) make great contributions to the pathogenesis of ulcerative colitis (UC). In our study, 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid (BT2) exerted significant therapeutic effects on the amelioration of dextran sodium sulfate-induced acute colitis. Our work reported that BT2 played an anti-UC role through suppression of branched amino acid-associated mTORC1 activation and modulation of the intestinal flora. Overall, BT2 could represent a potential candidate drug in the design of treatment strategies for UC.