急性胰腺炎(AP),作为临床急腹症的常见原因,往往导致多器官损伤。在严重AP的过程中,除了胰腺,肺和肠是最容易受影响的器官。这些器官损害相继发生。值得注意的是,肺和肠道损伤密切相关。对ML的损害,它运输免疫细胞,肠液,Chyle,和有毒成分(包括毒素,胰蛋白酶,和激活的细胞因子到AP中的体循环)可以连接到AP。这一过程可导致肺高渗水肿的病理变化,肺泡液水平升高,肠粘膜结构的破坏,肠粘膜通透性受损。肺和肠损伤相关的潜在机制是炎症反应,氧化应激,和内分泌激素分泌紊乱。肺和肠损伤的主要信号通路是TNF-α,HMGB1介导的NF-κB信号通路的炎症扩增效应,Nrf2/ARE氧化应激反应信号通路,和IL-6介导的JAK2/STAT3信号通路。这些途径发挥抗炎反应和抗氧化应激,抑制细胞增殖,促进细胞凋亡。这种相互作用符合中医关于肺与大肠相连的理论(中文为飞宇达昌翔标利)。本文旨在探讨AP中肺和肠损伤的交叉机制,以开发新的治疗策略。
Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are closely linked. Damage to ML, which transports immune cells, intestinal fluid, chyle, and toxic components (including toxins, trypsin, and activated cytokines to the systemic circulation in AP) may be connected to AP. This process can lead to the pathological changes of hyperosmotic edema of the lung, an increase in alveolar fluid level, destruction of the intestinal mucosal structure, and impairment of intestinal mucosal permeability. The underlying mechanisms of the correlation between lung and intestinal injuries are inflammatory response, oxidative stress, and endocrine hormone secretion disorders. The main signaling pathways of lung and intestinal injuries are TNF-α, HMGB1-mediated inflammation amplification effect of NF-κB signal pathway, Nrf2/ARE oxidative stress response signaling pathway, and IL-6-mediated JAK2/STAT3 signaling pathway. These pathways exert anti-inflammatory response and anti-oxidative stress, inhibit cell proliferation, and promote apoptosis. The interaction is consistent with the traditional Chinese medicine theory of the lung being connected with the large intestine (fei yu da chang xiang biao li in Chinese). This
review sought to explore intersecting mechanisms of lung and intestinal injuries in AP to develop new treatment strategies.