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Chinese Journal of Experimental Traditional Medical Formulae ; (24): 232-241, 2023.
Artigo em Chinês | WPRIM | ID: wpr-976558

RESUMO

Ulcerative colitis (UC) is a common inflammatory bowel disease (IBD) in clinical practice, characterized by symptoms such as abdominal pain, diarrhea, and bloody mucus in the stool. It is difficult to cure and has a high recurrence rate. The pathogenesis of UC is related to abnormal immune response, oxidative stress in intestinal tissues, and inflammatory reactions. As reported, the abnormal activation of the NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome is involved in the pathological process of UC. This activation triggers pathological mechanisms such as oxidative stress, pyroptosis, and inflammation in intestinal epithelial cells. Therefore, blocking the abnormal activation of NLRP3 is beneficial for alleviating UC. Currently, western medicine treatment for UC mainly includes salicylic acid derivatives, corticosteroids, and biologics, but the overall efficacy is unsatisfactory. Traditional Chinese medicine (TCM) treatment of this disease has the advantages of significant efficacy and low recurrence rate. In recent years, great advances have been made in the basic research of using TCM methods to treat UC. Studies have found that TCM intervention targeting the NLRP3 inflammasome can significantly promote intestinal mucosal healing and treat UC, and the mechanism of action involves multiple targets, levels, and pathways. This article summarized the experimental research on the impact of TCM targeting the NLRP3 inflammasome on UC in recent years, and found that NLRP3 interacted with factors such as Caspase-1 and nuclear factor-κB (NF-κB), thereby promoting the release of pro-inflammatory factors and cell pyroptosis in intestinal epithelial cells. This activation triggered oxidative stress, inflammatory reactions, and other pathological mechanisms. TCM acted on the NLRP3 inflammasome and its upstream and downstream factors to block the pathological process of UC, inhibit the pathological damage to the intestinal mucosa, and thereby alleviate colonic ulcers. The findings of this study provide a theoretical basis for the prevention and treatment of UC and further drug development.

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