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目的探讨NF-κB在重症急性胰腺炎小鼠肠黏膜屏障功能损伤中的调控机制。方法 36只BALB/C小鼠随机分为对照组、模型组、NF-κB干预组,每组12只。18h后处死小鼠,比较各组的腹腔内大体改变、肠黏膜病理改变,肠道通透性的变化及血清细胞因子水平,肠上皮紧密连接蛋白occludin的表达。结果模型组小鼠腹腔内呈明显炎症反应,肠管水肿,肠黏膜水肿,肠道通透性显著增高,NF-κB特异性阻断剂能降低肠道损伤,改善肠黏膜水肿,上调肠上皮紧密连接蛋白occludin的表达,显著降低肠道通透性,降低细胞因子水平。结论 NF-κB阻断剂能够通过选择性的抑制NF-κB活性,改善受损的肠屏障功能。这一作用通过上调肠上皮紧密连接蛋白occludin的水平而实现。
Objective To investigate the regulatory mechanism of NF-κB in the intestinal mucosal barrier dysfunction in severe acute pancreatitis in mice. Methods Thirty-six BALB / C mice were randomly divided into control group, model group and NF-κB intervention group, with 12 rats in each group. After 18 hours, the mice were sacrificed. The intraperitoneal changes, the pathological changes of intestinal mucosa, the changes of intestinal permeability, the level of serum cytokines and the expression of occludin in intestinal epithelium were compared. Results The mice in the model group showed obvious inflammatory reaction in abdominal cavity, intestinal edema, intestinal mucosa edema and intestinal permeability were significantly increased. NF-κB specific antagonist could reduce intestinal damage, improve intestinal mucosal edema, The expression of connexin occludin significantly reduced intestinal permeability and decreased cytokine levels. Conclusion NF-κB blockers can improve impaired intestinal barrier function by selectively inhibiting NF-κB activity. This effect is achieved by up-regulating the level of intestinal tight junction protein occludin.