Jin-Wei Zhao,1 Lu-Yao Li,1 Fang-Wang Ye,1 Wei-Yi Zhao2 

1Department of Hepatopancreatobiliary Surgery, The Second Hospital of Jilin University, Changchun, Jilin, 130022, People’s Republic of China; 2Medical College of Yanbian University, Yanbian, Jilin, 133002, People’s Republic of China

Correspondence: Wei-Yi Zhao, Medical College of Yanbian University, 977 Park Road, Yanji, Jilin, 133002, People’s Republic of China, Tel +86 15843112824, Email zhaoweiyiwyz@outlook.com

Abstract: Ulcerative colitis (UC) is a form of non-specific inflammatory bowel disease characterized by complex pathological mechanisms that remain incompletely understood, posing challenges for effective treatment. Pyroptosis, a form of inflammatory cell death mediated by the Gasdermin D protein family, occurs primarily through the classical caspase-1 pathway, the non-classical caspase-4, 5, and 11 pathways, and alternative pathways. Dysregulated activation of pyroptosis signaling has been implicated in the progression of UC, indicating that targeted inhibition of pyroptosis may serve as a therapeutic strategy. Food-derived compounds have demonstrated promise in modulating key pyroptosis-related targets, thereby providing potential therapeutic benefits for UC. This review examines the classical, non-classical, and alternative pathways of pyroptosis and their roles in UC pathogenesis and treatment. Additionally, the effects and mechanisms of action of natural compounds in targeting programmed cell death are discussed, with the aim of informing future therapeutic strategies and contributing to the development of new pharmacological interventions for UC.

Keywords: food-derived compounds, inflammation, mechanism, pyroptosis, UC