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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。
Objective To observe the relationship between bacterial translocation and the expression of gelatinase-associated lipocalin (NGAL) in the model of liver cirrhosis and provide a reference for clinical treatment. Methods Sixty male Sprague-Dawley rats were used as control. Fifty male Sprague-Dawley rats were used as blank control. Fifty-five SD male rats were induced with carbon tetrachloride (CCl4) to induce cirrhosis and ascites. Bacterial culture and bacterial DNA sequencing were used to detect the mesentery Bacterial species of lymph node translocation and translocation were detected. PCR was used to detect bacterial DNA translocation. Immunohistochemistry and Western blot were used to detect the expression of NGAL in intestinal mucosa. Results Immunohistochemistry showed that the expression of NGAL in intestinal mucosa during bacterial translocation was significantly higher than that in bacterial translocation group and no translocation group or control group (P <0.05) Bacterial DNA translocation group expression than bacterial translocation group or control group (P <0.05). Conclusions The increase of intestinal mucosal expression of NGAL during bacterial translocation may inhibit the bacterial translocation by inhibiting the intestinal absorption of intestinal bacteria and promoting the repair of intestinal mucosa. This may be one of the mechanisms involved in the inhibition of bacterial translocation.