Yang BL, Zhu P, Li YR, Xu MM, Wang H, Qiao LC, Xu HX, Chen HJ. Total flavone of Abelmoschus manihot suppresses epithelial-mesenchymal transition via interfering transforming growth factor-β1 signaling in Crohn’s disease intestinal fibrosis. World J Gastroenterol 2018; 24(30): 3414-3425 [PMID: 30122880 DOI: 10.3748/wjg.v24.i30.3414]
Corresponding Author of This Article
Hong-Jin Chen, MD, Chief Doctor, Department of Colorectal Surgery, The Affiliated Hospital of Nanjing University of Chinese Medicine, Hanzhong 155 Rd, Nanjing 210029, Jiangsu Province, China. 260789@njucm.edu.cn
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Aug 14, 2018; 24(30): 3414-3425 Published online Aug 14, 2018. doi: 10.3748/wjg.v24.i30.3414
Total flavone of Abelmoschus manihot suppresses epithelial-mesenchymal transition via interfering transforming growth factor-β1 signaling in Crohn’s disease intestinal fibrosis
Bo-Lin Yang, Ping Zhu, You-Ran Li, Min-Min Xu, Hao Wang, Li-Chao Qiao, Hai-Xia Xu, Hong-Jin Chen, Department of Colorectal Surgery, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, Jiangsu Province, China
Author contributions: Yang BL and Chen HJ contributed to the conception and design of the study, acquisition, analysis and interpretation of data; all authors drafted the article and made critical revisions, and approved the final version of the article to be published.
Supported bythe Natural Science Foundation of Jiangsu Province, China, No. BK2016157; the National Natural Science Foundation of China, No. 81673973; Phase II Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions, No. 035062002003; and Developing Program for High-level Academic Talent in Jiangsu Hospital of TCM, No. y2018rc16.
Conflict-of-interest statement: To the best of our knowledge, no conflict of interest exists.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Hong-Jin Chen, MD, Chief Doctor, Department of Colorectal Surgery, The Affiliated Hospital of Nanjing University of Chinese Medicine, Hanzhong 155 Rd, Nanjing 210029, Jiangsu Province, China. 260789@njucm.edu.cn
Telephone: +86-13851887158
Received: May 10, 2018 Peer-review started: May 10, 2018 First decision: June 11, 2018 Revised: June 27, 2018 Accepted: June 28, 2018 Article in press: June 28, 2018 Published online: August 14, 2018 Processing time: 95 Days and 17.6 Hours
Core Tip
Core tip: Regulating transforming growth factor-β (TGF-β) and its downstream signaling pathways, mediating the epithelial-mesenchymal transition (EMT) process and restoring the biological function of abnormally activated intestinal fibroblasts, may be an important way to seek drug therapy for Crohn’s disease (CD) intestinal fibrosis. Total flavone of Abelmoschus manihot (TFA) can inhibit TGF-β1-induced morphological change, migration, invasion of rat intestinal epithelial cells, and promote induction of EMT partially by inhibiting TGF-β1-activated Smad and non-Smad signaling pathways. Therefore, TFA is expected to advance as a new therapy to treat CD intestinal fibrosis, and its continued advancement may open the door to a new class of treatment for CD intestinal fibrosis.
