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目的 探讨N (2)-L-丙氨酰-L-谷氨酰胺(NLAG)对失血性休克大鼠肠黏膜屏障的作用及其对TLR4/Myd88信号通路表达的影响.方法 清洁级SD大鼠30只,随机分为假手术组(Sham)、失血性休克组(HS)和NLAG组,每组10只.按大鼠总血容量35％放血建立HS模型,HS组自体血回输复苏,NLAG组于HS后腹腔注射NLAG.于HS发生后4h处死大鼠,观察小肠组织病理学结果;检测血中肠脂肪酸结合蛋白(I-FABP)和D-乳酸浓度;ELISA检测血清中TNF-α、IL-6、IL-10浓度;Westem-blot法检测TLR4、Myd88、NF-κB蛋白表达水平.结果 NLAG抑制脓毒症引发的全身炎症反应,降低血浆中I-FABP、D-乳酸含量,下调血浆中TNF-,IL-6和IL-10含量;抑制肠损伤,改善肠屏障功能,降低肠粘膜TLR4、Myd88、NF-κ B蛋白表达水平.结论 NLAG抑制HS大鼠肠黏膜损伤可能与下调炎症因子和TLR4/Myd88信号通路有关“,”Objective To investigate the inhibitory effect of N (2)-L-alanyl-L-glutamine(NLAG) on intestinal mucosal injury in rats with hemorrhagic shock.Methods 30 SD rats were randomly divided into sham group(Sham),hemorrhagic shock group(HS) and N (2)-L-alanyl-L-glutamine group(NLAG).The pathological chang was observed by HE staining,blood intestinal fatty acid binding protein (I-FABP) and D-ELISA were determined,concentrations of TNF-,IL-6,IL alpha-10 in serum were detected by ELISA,TLR4,Myd88,NF-kappa B protein expressions in intestinal mucus were detected by Western-blot.Results NLAG inhibited the systemic infflammatory response induced by sepsis,inhibited intestinal injury,improved intestinal barrier function,reduced plasma I-FABP,Dlactic acid concentrations,downregulated concentrations of TNF-,IL-6 and IL-10 in rat plasma and expression levels of TLR4,Myd88,NF-kappa B in intestinal mucus.Conclusion The inhibition of NLAG on the intestinal mucosal injury of HS ratsmight be related to the decrease of inflammation factors and TLR4/Myd88 signaling pathway.