Basic Study
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 14, 2021; 27(46): 7982-7994
Published online Dec 14, 2021. doi: 10.3748/wjg.v27.i46.7982
Recombinant protein Schistosoma japonicum-derived molecule attenuates dextran sulfate sodium-induced colitis by inhibiting miRNA-217-5p to alleviate apoptosis
Li-Chao Zhang, Xiao-Ying Wu, Rui-Bing Yang, Fang Chen, Jia-Hua Liu, Yun-Yi Hu, Zhong-Dao Wu, Li-Fu Wang, Xi Sun
Li-Chao Zhang, Rui-Bing Yang, Jia-Hua Liu, Yun-Yi Hu, Zhong-Dao Wu, Xi Sun, Department of Parasitology of Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510000, Guangdong Province, China
Xiao-Ying Wu, Department of Gastroenterology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Fang Chen, School of Medicine, South China University of Technology, South China University of Technology, Guangzhou 510000, Guangdong Province, China
Li-Fu Wang, Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China
Author contributions: Sun X contributed to the experiment design; Wu ZD, Yang RB, and Chen F contributed to the experiment implementation; Liu JH and Hu YY analyzed the data; Zhang LC and Wang LF conceived the experiments, performed the experiments, and wrote the manuscript; all authors participated in critical revision of the manuscript and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 81902081 and No. 81871682; the Natural Science Foundation of Guangdong Province, No. 2020A1515011573 and No. 2019A1515012068; China Postdoctoral Science Foundation, No. 2018M640858 and No. 2019T120771; Fundamental Research Funds for the Central Universities, No. 19ykpy170, No. 17ykpy09 and No. 19ykpy29; National Science and Technology Major Project, No. 2018ZX10101002-001; the 111 Project, No. B12003; and the Natural Science Foundation of Guangdong Province, No. 2021A1515010976.
Institutional review board statement: The study was reviewed and approved by the Sun Yat-sen University Institutional Review Board.(Approval No. SYSU-IACUC-2019-B517).
Conflict-of-interest statement: The authors declare no competing interests.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: I 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: Li-Fu Wang, DO, Research Scientist, Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, No. 74 Zhongshan Road, Guangzhou 510080, Guangdong Province, China. wanglf99999@163.com
Received: June 16, 2021
Peer-review started: June 16, 2021
First decision: June 30, 2021
Revised: July 9, 2021
Accepted: November 29, 2021
Article in press: November 29, 2021
Published online: December 14, 2021
Processing time: 176 Days and 23.1 Hours
ARTICLE HIGHLIGHTS
Research background

Inflammatory bowel disease (IBD) encompasses Crohn’s disease, ulcerative colitis and IBD-unclassified. Although newer treatments have increased the chances of remission, most IBD patients cannot maintain remission, and death is not an infrequent outcome of IBD. Therefore, it is very important to explore the pathogenesis of IBD and to find effective therapeutic targets.

Research motivation

Exploring the pathogenesis of IBD and to find effective therapeutic targets.

Research objectives

To apoptosis and its mechanism.

Research methods

In-vivo, after DSS inducing colitis. The severity of colitis was assessed. WB was used to detect the changes of apoptosis-related genes in colon tissues. In-vitro, WB, Qpcr and tunel was used to detect the changes of apoptosis.

Research results

rSj16 attenuates clinical activity in DSS-induced colitis mice. rSj16 could reduce the expression of miR-217-5p in MODE-K cells. rSj16 could regulate the apoptosis of MODE-K cells.

Research conclusions

rSj16 attenuates IBD in mice by regulating the miR-217-5p/ HNF1B axis.

Research perspectives

miR-217-5p and HNF1B may be potential biomarkers to improve the accuracy of IBD diagnosis and treatment, and that rSj16 may have potential for clinical drug development.