Department of Gastroenterology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052, China.
Hebei North University, Zhangjiakou 075000, China.
Mediators Inflamm. 2021 Feb 15;2021:1315797. doi: 10.1155/2021/1315797. eCollection 2021.
Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1 and 7 day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-B), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF--induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection.
中风是全球第二大致死原因。中风患者易发生多种胃肠道 (GI) 并发症，如吞咽困难、GI 出血和大便失禁。然而，目前针对中风后胃肠道的研究较少。本研究旨在探讨缺血性中风后小鼠肠道结构和功能的变化。采用大脑中动脉闭塞 (MCAO) 制作中风疾病模型，分别在中风后第 1 天和第 7 天收集大脑和回肠组织进行实验。结果显示，中风后小鼠的肠道运动受到抑制，肠道通透性增加。苏木精-伊红 (HE) 染色显示肠黏膜白细胞积聚。中风后，小鼠小肠中的髓过氧化物酶 (MPO) 活性和炎症蛋白（核因子 kappa-B (NF-B)、诱导型一氧化氮合酶 (iNOS)）显著增加。紧密连接 (TJ) 蛋白（闭合蛋白-1 (ZO-1)、闭合蛋白和 Claudin-1）的表达下调，电镜显示中风后肠黏膜 TJ 断裂。胶质纤维酸性蛋白 (GFAP) 和凋亡相关蛋白（肿瘤坏死因子 (TNF-α)、半胱氨酸天冬氨酸蛋白酶-3 (caspase-3) 和 cleaved caspase-3）也明显上调。缺血性中风导致肠道结构和功能发生负性变化。炎症介质和 TNF-α 诱导的死亡受体信号通路可能参与其中，破坏小肠屏障功能。这些结果表明，中风患者应注意胃肠道保护。
