| 引用本文: |
黄晓旭, 吴文杰, 胡响当, 鲁海燕.基于“亢害承制”理论探讨巨噬细胞极化在溃疡性结肠炎发展中的作用[J].湖南中医药大学学报,2025,45(12):2379-2384[点击复制] |
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| 基于“亢害承制”理论探讨巨噬细胞极化在溃疡性结肠炎发展中的作用 |
| 黄晓旭,吴文杰,胡响当,鲁海燕 |
| (湖南中医药大学, 湖南 长沙 410208;湖南中医药大学第二附属医院, 湖南 长沙 410005) |
| 摘要: |
| 溃疡性结肠炎（UC）是一种主要累及结肠黏膜及其下层的一种慢性非特异性炎症性肠病。巨噬细胞对肠道微环境和炎症反应的调控在UC的疾病进展中至关重要。“亢害承制”作为中医的核心理论之一，系统阐释了人体内部生克关系的动态平衡、病理失衡的本质及其演变规律，并为临床辨证施治提供了关键指导法则。脾虚失运导致水湿停滞、清浊相混，久羁郁热化毒，浊毒壅滞肠腑，蚀伤脂膜络脉致气血腐败，形成新的致病因素损害机体。这与UC肠道巨噬细胞极化状态由M2型向M1型偏移引发肠黏膜屏障显著受损、炎性介质过度生成与释放、免疫细胞异常聚集浸润、肠上皮结构及功能完整性破坏等病理变化机制高度吻合。基于“亢害承制”理论，确立“健脾益气以强化承制之功，解毒化浊以平抑亢盛之邪”基本治则，旨在重建M1/M2型巨噬细胞平衡，恢复肠道微环境稳态，缓解肠道炎症及损伤黏膜，以期为UC的临床防治提供潜在的新策略。 |
| 关键词: 溃疡性结肠炎 巨噬细胞极化 亢害承制 脾虚 浊毒 动态平衡 |
| DOI：10.3969/j.issn.1674-070X.2025.12.019 |
| 投稿时间：2025-08-25 |
| 基金项目:湖南省自然科学基金高校联合基金项目（2025JJ90122）；湖南中医药大学校级联合基金重点项目（2021XJJJ054）；湖南省中医药管理局委托课题重点项目（D2023008）；湖南省卫生健康委员会科研计划项目重点课题（C202304017114）。 |
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| Role of macrophage polarization in ulcerative colitis development based on the "harmful hyperactivity and responding inhibition" theory |
| HUANG Xiaoxu, WU Wenjie, HU Xiangdang, LU Haiyan |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;The Second Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410005, China) |
| Abstract: |
| Ulcerative colitis (UC) is a chronic non-specific inflammatory bowel disease primarily affecting the colonic mucosa and submucosa. Macrophages play a crucial role in regulating the intestinal microenvironment and inflammatory response during UC progression. The "harmful hyperactivity and responding inhibition" theory, one of the core theories in Chinese medicine, systematically elucidates the dynamic equilibrium of engendering and restraining relationships within the human body, the nature of pathological imbalance, and its evolutionary patterns, providing key guiding principles for clinical pattern differentiation and treatment. Spleen deficiency with impaired transportation leads to water-dampness retention and intermingling of the clear and turbid phases. Prolonged retention causes depression transforming into heat and toxins, resulting in turbidity and toxin congesting the intestinal fu-organ, eroding the adipose membrane and collaterals, and causing corruption of qi and blood, thereby forming new pathogenic factors that damage the body. This pathogenesis closely corresponds to the pathological mechanisms observed in UC, in which a shift in intestinal macrophage polarization from the M2 to the M1 phenotype triggers significant damage to the intestinal mucosal barrier, excessive production and release of inflammatory mediators, abnormal aggregation and infiltration of immune cells, and disruption of the structural and functional integrity of the intestinal epithelium. Based on the "harmful hyperactivity and responding inhibition" theory, the fundamental treatment principle of "strengthening the spleen and tonifying qi to enhance its restraining function, and removing toxins and transforming turbidity to suppress hyperactive pathogenic factors" has been established. This approach aims to rebalance M1/M2 macrophage polarization, restore the homeostasis of the intestinal microenvironment, and alleviate intestinal inflammation and mucosal injury, thereby potentially offering a novel strategy for the clinical prevention and treatment of UC. |
| Key words: ulcerative colitis macrophage polarization harmful hyperactivity and responding inhibition spleen deficiency turbidity and toxin dynamic equilibrium |
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