Ali FE, Ibrahim IM, Ghogar OM, Abd-alhameed EK, Althagafy HS, Hassanein EH. Therapeutic interventions target the NLRP3 inflammasome in ulcerative colitis: Comprehensive study. World J Gastroenterol 2023; 29(6): 1026-1053 [PMID: 36844140 DOI: 10.3748/wjg.v29.i6.1026]
Corresponding Author of This Article
Fares E.M Ali, MSc, PhD, Lecturer, Research Scientist, Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Al-Azhar Street, Assiut 71524, Egypt. faresali@azhar.edu.eg
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
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. Feb 14, 2023; 29(6): 1026-1053 Published online Feb 14, 2023. doi: 10.3748/wjg.v29.i6.1026
Therapeutic interventions target the NLRP3 inflammasome in ulcerative colitis: Comprehensive study
Fares E.M Ali, Islam M. Ibrahim, Osama M Ghogar, Esraa K. Abd-alhameed, Hanan S. Althagafy, Emad H.M. Hassanein
Fares E.M Ali, Emad H.M. Hassanein, Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Assiut 71524, Egypt
Islam M. Ibrahim, Osama M Ghogar, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Assiut 71524, Egypt
Esraa K. Abd-alhameed, Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef 12345, Egypt
Hanan S. Althagafy, Department of Biochemistry, Faculty of Science, University of Jeddah, Jeddah 12345, Saudi Arabia
Author contributions: Ali FE and Hassanein EH designed and critically wrote the manuscript; Ibrahim IM, Ghogar OM, and Abd-alhameed EK collected data, and drafted the manuscript; Althagafy HS contributed to manuscript revision and proof editing.
Conflict-of-interest statement: There are no conflicts of interest to report.
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: Fares E.M Ali, MSc, PhD, Lecturer, Research Scientist, Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Al-Azhar Street, Assiut 71524, Egypt. faresali@azhar.edu.eg
Received: November 19, 2022 Peer-review started: November 19, 2022 First decision: November 30, 2022 Revised: December 29, 2023 Accepted: January 29, 2023 Article in press: January 29, 2023 Published online: February 14, 2023
Abstract
One of the significant health issues in the world is the prevalence of ulcerative colitis (UC). UC is a chronic disorder that mainly affects the colon, beginning with the rectum, and can progress from asymptomatic mild inflammation to extensive inflammation of the entire colon. Understanding the underlying molecular mechanisms of UC pathogenesis emphasizes the need for innovative therapeutic approaches based on identifying molecular targets. Interestingly, in response to cellular injury, the NLR family pyrin domain containing 3 (NLRP3) inflammasome is a crucial part of the inflammation and immunological reaction by promoting caspase-1 activation and the release of interleukin-1β. This review discusses the mechanisms of NLRP3 inflammasome activation by various signals and its regulation and impact on UC.
Core Tip: Ulcerative colitis (UC) is a common chronic type of inflammatory bowel disease that affects a significant number of populations. Needing to counteract the UC prevalence, attract scientists to study its pathological mechanism deeply. NLR family pyrin domain containing 3 (NLRP3) inflammasome has been observed to have a crucial role in the pathological features of UC. Targeting NLRP3 inflammasome signals with phytochemicals, plants, probiotics, and chemical agents could be promising candidates for fixing the UC problem.
