Zhao Jin-Wei, Li Lu-Yao, Ye Fang-Wang, Zhao Wei-Yi
Department of Hepatopancreatobiliary Surgery, The Second Hospital of Jilin University, Changchun, Jilin, 130022, People's Republic of China.
Medical College of Yanbian University, Yanbian, Jilin, 133002, People's Republic of China.
J Inflamm Res. 2025 Aug 27;18:11667-11688. doi: 10.2147/JIR.S531820. eCollection 2025.
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.
溃疡性结肠炎(UC)是一种非特异性炎症性肠病,其病理机制复杂,尚未完全明确,这给有效治疗带来了挑战。细胞焦亡是一种由Gasdermin D蛋白家族介导的炎症性细胞死亡形式,主要通过经典的半胱天冬酶-1途径、非经典的半胱天冬酶-4、5和11途径以及替代途径发生。细胞焦亡信号的失调激活与UC的进展有关,这表明靶向抑制细胞焦亡可能是一种治疗策略。食物衍生化合物已显示出调节关键细胞焦亡相关靶点的潜力,从而为UC提供潜在的治疗益处。本综述探讨了细胞焦亡的经典、非经典和替代途径及其在UC发病机制和治疗中的作用。此外,还讨论了天然化合物在靶向程序性细胞死亡方面的作用效果和机制,旨在为未来的治疗策略提供参考,并为UC新药理学干预措施的开发做出贡献。