Progress on Regulation of NLRP3 Inflammasome by Chinese Medicine in Treatment of Ulcerative Colitis.
10.1007/s11655-023-3551-1
- Author:
Hao-Xian SUN
1
;
Ying ZHU
2
Author Information
1. Department of Gastroenterology, the First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China.
2. Department of Gastroenterology, the First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China. bjdf1992@126.com.
- Publication Type:Review
- Keywords:
Chinese medicine;
NLRP3 inflammasome;
mechanism of action;
review;
ulcerative colitis
- MeSH:
Humans;
Inflammasomes/metabolism*;
Colitis, Ulcerative/pathology*;
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism*;
Medicine, Chinese Traditional;
Quality of Life;
Colitis
- From:
Chinese journal of integrative medicine
2023;29(8):750-760
- CountryChina
- Language:English
-
Abstract:
Ulcerative colitis (UC) is a chronic, non-specific intestinal disease that not only affects the quality of life of patients and their families but also increases the risk of colorectal cancer. The nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome is an important component of inflammatory response system, and its activation induces an inflammatory cascade response that is involved in the development and progression of UC by releasing inflammatory cytokines, damaging intestinal epithelial cells, and disrupting the intestinal mucosal barrier. Chinese medicine (CM) plays a vital role in the prevention and treatment of UC and is able to regulate NLRP3 inflammasome. Many experimental studies on the regulation of NLRP3 inflammasome mediated by CM have been carried out, demonstrating that CM formulae with main effects of clearing heat, detoxifying toxicity, drying dampness, and activating blood circulation. Flavonoids and phenylpropanoids can effectively regulate NLRP3 inflammasome. Other active components of CM can interfere with the process of NLRP3 inflammasome assembly and activation, leading to a reduction in inflammation and UC symptoms. However, the reports are relatively scattered and lack systematic reviews. This paper reviews the latest findings regarding the NLRP3 inflammasome activation-related pathways associated with UC and the potential of CM in treating UC through modulation of NLRP3 inflammasome. The purpose of this review is to explore the possible pathological mechanisms of UC and suggest new directions for development of therapeutic tools.
