VAGUS NERVE STIMULATION ATTENUATES INTESTINAL EPITHELIAL TIGHT JUNCTIONS DISRUPTION IN ENDOTOXEMIC MICE THROUGH alpha 7 NICOTINIC ACETYLCHOLINE RECEPTORS
文献类型:期刊论文
作者 | Zhou, Hui1; Liang, Hui2; Li, Zhi-Feng1; Xiang, Hui1; Liu, Wei3; Li, Jian-Guo1 |
刊名 | SHOCK |
出版日期 | 2013-08-01 |
卷号 | 40期号:2页码:144-151 |
ISSN号 | 1073-2322 |
关键词 | alpha 7 nicotinic acetylcholine receptor tight junction endotoxemia myosin light chain kinase NF-kappa B alpha-bungarotoxin |
中文摘要 | We tested the effect of vagus nerve stimulation in endotoxin-induced intestinal tight junction injury in mice challenged with lipopolysaccharide (LPS) and examined the role of alpha 7 nicotinic acetylcholine receptors (alpha 7nAchR) in this process. Endotoxemia was induced by intraperitoneal injection of LPS (10 mg/kg) in male Balb/c mice. Samples were collected 12 h after LPS treatment. Endotoxemia was associated with intestinal barrier dysfunction, as evidenced by increased amount of fluorescein isothiocyanate-dextran in circulation. Western blot and immunofluorescence was performed, and the results demonstrated decreased expression of occludin and zonula occludens 1 along intestinal epithelium in endotoxemic mice. The ultrastructure of tight junction was disrupted as shown by transmission electron microscopy, which was associated with increased intestinal permeability. Stimulation of the right cervical vagus nerve ameliorated the damage of tight junction ultrastructure, which was consistent with decreased permeability to fluorescein isothiocyanate-dextran, and also reversed the decreased expression of tight junction proteins occludin and zonula occludens 1. Vagus nerve stimulation inhibited the upregulated activity of myosin light chain kinase and nuclear factor kappa B. In contrast, alpha-bungarotoxin (a specific alpha 7nAchR antagonist, 0.1 mu g/mouse) administered before vagus nerve stimulation significantly abolished these protective effects of vagus nerve stimulation. Our results for the first time confirmed that vagus nerve stimulation attenuated the disruption of tight junction in intestinal epithelium in endotoxemic mice, which was mediated through suppressing translocation of nuclear factor kappa B p65, downregulating myosin light chain kinase, and the alpha 7nAchR may play an important role in this process. |
英文摘要 | We tested the effect of vagus nerve stimulation in endotoxin-induced intestinal tight junction injury in mice challenged with lipopolysaccharide (LPS) and examined the role of alpha 7 nicotinic acetylcholine receptors (alpha 7nAchR) in this process. Endotoxemia was induced by intraperitoneal injection of LPS (10 mg/kg) in male Balb/c mice. Samples were collected 12 h after LPS treatment. Endotoxemia was associated with intestinal barrier dysfunction, as evidenced by increased amount of fluorescein isothiocyanate-dextran in circulation. Western blot and immunofluorescence was performed, and the results demonstrated decreased expression of occludin and zonula occludens 1 along intestinal epithelium in endotoxemic mice. The ultrastructure of tight junction was disrupted as shown by transmission electron microscopy, which was associated with increased intestinal permeability. Stimulation of the right cervical vagus nerve ameliorated the damage of tight junction ultrastructure, which was consistent with decreased permeability to fluorescein isothiocyanate-dextran, and also reversed the decreased expression of tight junction proteins occludin and zonula occludens 1. Vagus nerve stimulation inhibited the upregulated activity of myosin light chain kinase and nuclear factor kappa B. In contrast, alpha-bungarotoxin (a specific alpha 7nAchR antagonist, 0.1 mu g/mouse) administered before vagus nerve stimulation significantly abolished these protective effects of vagus nerve stimulation. Our results for the first time confirmed that vagus nerve stimulation attenuated the disruption of tight junction in intestinal epithelium in endotoxemic mice, which was mediated through suppressing translocation of nuclear factor kappa B p65, downregulating myosin light chain kinase, and the alpha 7nAchR may play an important role in this process. |
WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
类目[WOS] | Critical Care Medicine ; Hematology ; Surgery ; Peripheral Vascular Disease |
研究领域[WOS] | General & Internal Medicine ; Hematology ; Surgery ; Cardiovascular System & Cardiology |
关键词[WOS] | CHOLINERGIC ANTIINFLAMMATORY PATHWAY ; LIGHT-CHAIN KINASE ; BACTERIAL TRANSLOCATION ; HEMORRHAGIC-SHOCK ; BARRIER FUNCTION ; UNITED-STATES ; SEVERE SEPSIS ; IN-VIVO ; ACTIVATION ; INJURY |
资助信息 | National Natural Science Foundation of China [30972852] |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000330244400011 |
公开日期 | 2014-08-06 |
源URL | [http://ir.ihb.ac.cn/handle/342005/19987] |
专题 | 水生生物研究所_分析测试中心_期刊论文 |
作者单位 | 1.Wuhan Univ, Zhongnan Hosp, Dept Intens Care Unit, Wuhan 430071, Hubei Province, Peoples R China 2.Wuhan Univ, Renmin Hosp, Dept Anesthesiol, Wuhan 430071, Hubei Province, Peoples R China 3.Chinese Acad Sci, Inst Hydrobiol, Anal & Testing Ctr, Wuhan, Hubei Province, Peoples R China |
推荐引用方式 GB/T 7714 | Zhou, Hui,Liang, Hui,Li, Zhi-Feng,et al. VAGUS NERVE STIMULATION ATTENUATES INTESTINAL EPITHELIAL TIGHT JUNCTIONS DISRUPTION IN ENDOTOXEMIC MICE THROUGH alpha 7 NICOTINIC ACETYLCHOLINE RECEPTORS[J]. SHOCK,2013,40(2):144-151. |
APA | Zhou, Hui,Liang, Hui,Li, Zhi-Feng,Xiang, Hui,Liu, Wei,&Li, Jian-Guo.(2013).VAGUS NERVE STIMULATION ATTENUATES INTESTINAL EPITHELIAL TIGHT JUNCTIONS DISRUPTION IN ENDOTOXEMIC MICE THROUGH alpha 7 NICOTINIC ACETYLCHOLINE RECEPTORS.SHOCK,40(2),144-151. |
MLA | Zhou, Hui,et al."VAGUS NERVE STIMULATION ATTENUATES INTESTINAL EPITHELIAL TIGHT JUNCTIONS DISRUPTION IN ENDOTOXEMIC MICE THROUGH alpha 7 NICOTINIC ACETYLCHOLINE RECEPTORS".SHOCK 40.2(2013):144-151. |
入库方式: OAI收割
来源:水生生物研究所
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