中文摘要：

目的观察肝硬化模型中细菌移位与肠道中性粒细胞明胶酶相关脂质运载蛋白（NGAL）表达之间的关系,为临床治疗提供参考依据。方法选取60只SD雄性大鼠,其中5只SD雄性大鼠作为空白对照,55只SD雄性大鼠持续服用四氯化碳诱导形成肝硬化腹水模型,细菌培养及细菌DNA测序法,检测其肠系膜淋巴结细菌移位及移位后细菌的种类,PCR法检测细菌DNA移位情况,免疫组化法及Western blot法测定NGAL在肠道黏膜的表达。结果免疫组化检测提示肠道黏膜在细菌移位时有NGAL表达,且在MLN细菌移位组表达明显强于细菌DNA移位组及无移位组或对照组（P〈0.05）;NGAL在细菌DNA移位组表达又较无细菌移位组或对照组强（P〈0.05）。结论细菌移位时肠道黏膜表达NGAL增强可能通过抑制肠道细菌铁吸收并促进肠道黏膜的修复进而抑制细菌移位;这可能是机体参与抑制细菌移位的机制之一。

英文摘要：

OBJECTIVE To observe the relationship between the intestinal expression level of neutrophil gelatinaseassociated lipocalin（NGAL）and bacterial translocation（BT）in a rat liver cirrhosis model so as to provide reference for clinical treatments.METHODS A total of 60 rats were included in this experiment.Among them,5male Sprague Dawley（SD）rats were used as control group,other 55 male SD rats were induced into liver cirrhosis with ascites through periodic carbon tetrachloride intragastric administration.BT in the mesenteric lymph nodes（MLNs）of rats were detected by bacterial culture and bacterial DNA sequencing.Bacterial DNA in MLNs was evaluated using polymerase chain reaction.The expression level of NGAL in intestine mucosa was assessed by immunohistochemistry and Western blot.RESULTS Immunohistochemistry and Western blot indicated that high NGAL expression in the intestine mucosa of BT group compared to low expression in that of bacterial DNA translocation and non-translocation or control group（P〈0.05）.Furthermore,the expression of NGAL in the intestinal mucosa of bacterial DNA translocation group was also higher than that of non-translocation or control group（P〈0.05）.CONCLUSION Up-regulated expression of NGAL in the intestinal mucosa of BT rats may decrease bacteria amount of BT through inhibiting the iron metabolism of gut bacteria and promoting the repair of intestinal mucosa,which may be one of the mechanisms that hosts use to restrain BT.