首页> 外文期刊>World Journal of Gastroenterology >Systemic phosphatidylcholine pretreatment protects canine esophageal mucosa during acute experimental biliary reflux.
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Systemic phosphatidylcholine pretreatment protects canine esophageal mucosa during acute experimental biliary reflux.

机译:全身性磷脂酰胆碱预处理可在急性实验性胆汁反流期间保护犬食道粘膜。

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AIM: To characterize the consequences of short-term exposure to luminal bile on mucosal mast cell reactions in a canine model, and to determine the effects of systemic phosphatidylcholine pretreatment in this condition. METHODS: Twenty mongrel dogs were used for experiments. Group 1 (n = 5) served as a saline-treated control, while in group 2 (n = 5) the esophagus was exposed to bile for 3 h. In group 3 (n = 5) the animals were pretreated with 7-nitroindazole to inhibit the neuronal isoform of nitric oxide synthase. In group 4 (n = 5) phosphatidylcholine solution (50 mg/kg) was administered iv before the biliary challenge. Mucosal microcirculation was observed by intravital videomicroscopy. Myeloperoxidase and nitric oxide synthase activities, the degrees of mast cell degranulation and mucosal damage were evaluated via tissue biopsies. RESULTS: Exposure to bile evoked significant mast cell degranulation and leukocyte accumulation. The red blood cell velocity and the diameter of the postcapillary venules increased significantly. The tissue ATP content and constitutive nitric oxide synthase activity decreased, while the inducible nitric oxide synthase activity increased significantly as compared to the control values. 7-nitroindazole treatment significantly exacerbated the mucosal mast cell degranulation and tissue damage. In contrast, phosphatidylcholine pretreatment prevented the bile-induced ATP depletion, the inducible nitric oxide synthase and myeloperoxidase activity and the mast cell degranulation increased. CONCLUSION: The neuronal nitric oxide synthase--mast cell axis plays an important role in the esophageal mucosal defense system. Systemic phosphatidylcholine pretreatment affords effective protection through ameliorating the bile-induced ATP depletion and secondary inflammatory reaction.
机译:目的:在犬模型中表征短期暴露于腔内胆汁对粘膜肥大细胞反应的后果,并确定在这种情况下全身性磷脂酰胆碱预处理的作用。方法:20只杂种狗用于实验。第一组(n = 5)用作盐水处理的对照,而在第二组(n = 5)中,食道暴露于胆汁3 h。在第3组(n = 5)中,对动物进行7-硝基吲唑预处理以抑制一氧化氮合酶的神经元亚型。在第4组(n = 5)中,在胆道感染前静脉注射磷脂酰胆碱溶液(50 mg / kg)。通过活体视频显微镜观察粘膜微循环。通过组织活检评估髓过氧化物酶和一氧化氮合酶活性,肥大细胞脱粒程度和粘膜损伤程度。结果:暴露于胆汁引起肥大细胞脱粒和白细胞积聚。红细胞速度和毛细血管后小静脉的直径显着增加。与对照组相比,组织ATP含量和组成型一氧化氮合酶活性降低,而诱导型一氧化氮合酶活性显着提高。 7-硝基吲唑治疗显着加重了粘膜肥大细胞的脱粒和组织损伤。相反,磷脂酰胆碱预处理可防止胆汁诱导的ATP消耗,诱导型一氧化氮合酶和髓过氧化物酶活性以及肥大细胞脱颗粒增加。结论:神经元一氧化氮合酶-肥大细胞轴在食管粘膜防御系统中起重要作用。全身性磷脂酰胆碱预处理可通过改善胆汁诱导的ATP消耗和继发性炎症反应来提供有效的保护。

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