摘要
溃疡性结肠炎(ulcerative colitis,UC)是一种易复发、迁延难愈的慢性炎症性肠病,其发病机制尚未完全明确。文章从中医久病必瘀理论与现代医学铁死亡机制相结合的角度,探讨UC的作用机制。中医层面,“久病必瘀”导致的血瘀、痰浊、邪实等病理产物积聚是UC的核心病机;现代医学层面,铁死亡过程中的铁过载、脂质过氧化及GSH/GPX4抗氧化系统失衡,会破坏肠上皮细胞、损伤肠道屏障,引发肠道炎症。两者的病理机制高度契合,铁死亡的铁代谢、脂质代谢、氨基酸代谢紊乱分别对应久病必瘀的血瘀、痰瘀、正虚邪实核心病机。文章结合两者关联分析UC的发病过程,旨在为UC的临床治疗提供新的思路和方向。
Ulcerative colitis(UC)is a chronic inflammatory bowel disease that is prone to recurrence and difficult to cure,and its pathogenesis has not been fully clarified.This study explores the mechanism of UC from the perspective of combining the traditional Chinese medicine(TCM)theory of"chronic illness inevitably leads to blood stasis"with the modern medical mechanism of ferroptosis.At the TCM level,the accumulation of pathological products such as blood stasis,phlegm turbidity,and pathogenic excess caused by"chronic illness inevitably leads to blood stasis"is the core pathogenesis of UC;at the modern medical level,iron overload,lipid peroxidation,and imbalance of the GSH/GPX4 antioxidant system during ferroptosis can damage intestinal epithelial cells,impair the intestinal barrier,and trigger intestinal inflammation.The pathological mechanisms of the two are highly consistent:iron metabolism disorder,lipid metabolism disorder,and amino acid metabolism disorder in ferroptosis correspond to the core pathogenesis of blood stasis,phlegm-stasis,and deficiency of vital qi with excess of pathogenic factors in"chronic illness inevitably leads to blood stasis".This study analyzes the pathogenesis of UC by combining the correlation between the two,aiming to provide new ideas and directions for the clinical treatment of UC.
作者
邱东瑞
陈萌
QIU Dongrui;CHEN Meng(Liaoning University of Traditional Chinese Medicine,Shenyang 110847,Liaoning,China;The Third Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110003,Liaoning,China)
出处
《实用中医内科杂志》
2026年第3期22-26,共5页
Journal of Practical Traditional Chinese Internal Medicine
基金
国家自然科学基金青年科学基金项目(81804094)。
关键词
久病必瘀
铁死亡
溃疡性结肠炎
肠道屏障
脂质过氧化
chronic illness inevitably leads to blood stasis
ferroptosis
ulcerative colitis
intestinal barrier
lipid peroxidation
