Tang Xudong, Huang Yilin, Zhu Ying, Xu Yin
Department of Gastroenterology, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
First Clinical College, Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou, China.
Front Cell Dev Biol. 2025 Jun 5;13:1610435. doi: 10.3389/fcell.2025.1610435. eCollection 2025.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized primarily by immune dysregulation. Its pathogenesis involves multiple factors, including dysregulation of T-cell subsets, hypersecretion of pro-inflammatory cytokines, imbalance in the gut microbiota, and disruption of the intestinal barrier. Among T-cell subsets, abnormal activation of Th1 and Th17 cells, in conjunction with Treg dysfunction, significantly amplifies local pro-inflammatory signals. Pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-17, exacerbate apoptosis and disrupt tight junctions (TJs) in intestinal epithelial cells (IECs), thereby creating favorable conditions for invasion by pathogenic bacteria and their metabolites. Intestinal microecological imbalance not only leads to significant alterations in the structure of the bacterial flora but also involves abnormal fluctuations in its metabolites that directly regulate intestinal immune homeostasis, a factor closely associated with the severity of inflammation and prognosis of ulcerative colitis. Recent studies have demonstrated that in the treatment of UC, traditional Chinese medicine (TCM) achieves a multi-target, multi-pathway integrated intervention by regulating immune cell differentiation, balancing inflammatory factor levels, repairing the intestinal epithelial barrier, and remodeling the structure of the bacterial flora. This article reviews the pathogenic mechanisms underlying immune dysregulation in UC and the advances in research on TCM's role in immune regulation, anti-inflammatory repair, and flora modulation, encompassing the mechanisms of action of individual active ingredients and classic TCM compound formulas. Although some studies have preliminarily confirmed TCM's potential to modulate immunity and repair the intestinal barrier, breakthroughs in mechanism analysis, herb standardization, and large-scale validation remain forthcoming. It is anticipated that the unique advantages of TCM will be translated into a more precise therapeutic strategy for UC through modern molecular and systems biology approaches.
溃疡性结肠炎(UC)是一种主要以免疫失调为特征的慢性炎症性肠病(IBD)。其发病机制涉及多种因素,包括T细胞亚群失调、促炎细胞因子分泌过多、肠道微生物群失衡以及肠道屏障破坏。在T细胞亚群中,Th1和Th17细胞的异常激活,连同调节性T细胞(Treg)功能障碍,显著放大局部促炎信号。促炎细胞因子,如肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-17(IL-17),加剧细胞凋亡并破坏肠道上皮细胞(IEC)中的紧密连接(TJ),从而为病原菌及其代谢产物的侵入创造有利条件。肠道微生态失衡不仅导致细菌菌群结构的显著改变,还涉及直接调节肠道免疫稳态的代谢产物的异常波动,这一因素与溃疡性结肠炎的炎症严重程度和预后密切相关。最近的研究表明,在溃疡性结肠炎的治疗中,中药通过调节免疫细胞分化、平衡炎症因子水平、修复肠道上皮屏障和重塑细菌菌群结构,实现多靶点、多途径的综合干预。本文综述了溃疡性结肠炎免疫失调的发病机制以及中药在免疫调节、抗炎修复和菌群调节方面作用的研究进展,包括单个活性成分和经典中药复方的作用机制。尽管一些研究初步证实了中药调节免疫和修复肠道屏障的潜力,但在机制分析、草药标准化和大规模验证方面仍有待突破。预计通过现代分子和系统生物学方法,中药的独特优势将转化为更精确的溃疡性结肠炎治疗策略。