摘要
目的:观察类高血糖素多肽Ⅱ(GLP Ⅱ)对缺血再灌注所致的肠黏膜屏障损害的预防保护作用。 方法:采用夹闭肠系膜上动脉20min所致肠道缺血再灌注损伤小鼠模型,将30只小鼠随机分为正常(N)组、对照(C)组和GLP Ⅱ预处理(P)组。观察缺血再灌注后1天,肠黏膜形态、肠道细菌移位率、血浆内毒素水平和肠道IgA浓度的变化,并进行相关分析。 结果:缺血再灌注后,C组肠黏膜受到明显损伤,P组肠黏膜增生明显,C组和P组小鼠的肠道细菌移位率和血浆内毒素水平均明显高于N组(P<0. 01),肠道IgA浓度则明显降低(P<0. 01)。与C组相比,P组的细菌移位率和内毒素水平要低于C组(P=0. 005),IgA浓度要高于C组(P<0. 01)。 结论:缺血再灌注严重损害了肠黏膜屏障,经GLP Ⅱ预处理可以有效地减轻肠黏膜屏障的损伤。
Objective: To explore the protections of GLP-Ⅱ pretreatment on mouse intestinal mucosal immunity after ischemia/reperfusion insult. Methods: Thirty ICR mice were randomly divided into three groups: namely normal control (N), control (C) and GLP-Ⅱ pretreatment (P). Group C and group P were inflicted with ligation of superior mesenteric artery for twenty minutes. The morphology of distal ileum mucosa, the rate of intestinal bacteria translocation, the level of plasma endotoxin and intestinal IgA were determined. Results: After ischemia/reperfusion insult, there were obvious damage at distal ileum mucosa in group C and obvious proliferation in group P.The rate of intestinal bacteria translocation and the level of plasma endotoxin were significantly increased (P<0.01), and the levels of intestinal IgA were significantly decreased (P<0.01) in groups C and P. Comparing with group C, the rate of intestinal bacteria translocation and the level of plasma endotoxin were lower (P=0.005) and the levels of intestinal IgA were higher (P<0.01) in group P. Conclusion: The intestinal mucosal barrier may be severely damaged after ischemia/reperfusion insult. The preteatment of GLP-Ⅱ can relieve the damage of intestinal mucosal barrier.
出处
《肠外与肠内营养》
CAS
2005年第3期152-154,158,共4页
Parenteral & Enteral Nutrition
