急性胰腺炎患者肠黏膜屏障功能损害的相关性

Intestinal mucosal barrier dysfunction in patients with acute pancreatitis

目的:观察急性胰腺炎(acute pancreatitis,AP)患者肠黏膜屏障功能改变机制.方法:68例AP患者按病情程度分为重症组和轻症组,另35例健康志愿者作为对照组,电镜观察十二指肠肠黏膜超微结构变化,比较血清内毒素、白介素(interleukin,IL)-18、一氧化氮(nitric oxide,NO)及肠黏膜紧密连接蛋白(tight junction protein,ZO)-1、封闭蛋白(Occludin)的变化.结果:重症组ZO-1、Occludin蛋白染色变浅,重症组ZO-1、Occludin蛋白水平较对照组下降(0.31±0.010 vs 38±0.03,0.26±0.02 vs 0.34±0.02,P<0.05),血清内毒素、NO和IL-18含量较轻症组增高(0.39 EU/m L±0.05 EU/m L vs0.23 EU/m L±0.04 EU/m L,138.32μmol/L±27.49μmol/L vs 117.32μmol/L±19.23μmol/L,76.47 ng/L±19.37 ng/L vs 34.41 ng/L±16.33n g/L,P<0.05).血清内毒素、I L-18以及N O同ZO-1和Occludin蛋白光密度值呈负相关(P<0.05).结论:AP患者早期肠黏膜受损严重,肠黏膜通透性明显增加,部分细胞因子协同并促进肠黏膜的破坏.

AIM： To investigate the mechanism of intestinal mucosal barrier dysfunction in patients with acute pancreatitis（AP）. METHODS： Sixty-eight AP patients were divided into either a severe group or a mild group according to disease severity. Another 35 healthy volunteers were used as controls. Theultrastructural changes of the intestinal mucosa were observed by electron microscope. Serum levels of endotoxin, interleukin-18（IL-18） and nitric oxide（NO）, and expression of tight junction protein-1（ZO-1） and occludin in the intestinal mucosa were determined. RESULTS： The levels of ZO-1 and occludin protein expression in the severe group were significantly lower than those in the mild group（0.31 ± 0.010 vs 38 ± 0.03, 0.26 ± 0.02 vs 0.34 ± 0.02, P 〈 0.05）. Serum levels of endotoxin, NO and IL-18 in the severe group were significantly higher than those in the mild group（0.39 EU/m L ± 0.05 EU/m L vs 0.23 EU/m L ± 0.04 EU/m L, 138.32 μmol/L ± 27.49 μmol/L vs 117.32 μmol/L ± 19.23 μmol/L, 76.47 ng/L ± 19.37 ng/L vs 34.41 ng/L ± 16.33 ng/L, P 〈 0.05）. There were significant positive correlations among serum levels of endotoxin, IL-18, NO and intestinal expression of ZO-1 and occludin（P 〈 0.01）. CONCLUSION： Intestinal mucosa is damaged and intestinal permeability is increased in patients with AP. Some inflammatory mediators may participat in the pathogenesis of intestinal mucosal injury.