幽门螺杆菌下调人胃黏膜分泌性白细胞蛋白酶抑制因子的表达

Helicobacter pylori down-regulate expression of secretory leucocyte protease inhibitor in human gastric mucosa

目的通过低剂量阿斯匹林的处理作为炎性模型,研究分析人胃和十二指肠黏膜分泌性白细胞蛋白酶抑制因子(SLPI)表达下调是否与幽门螺杆菌(Helicobacter prlori,Hp)定居或感染有关.方法选择20例健康志愿者分成Hp+和Hp-组,其中Hp+组成功进行了根除治疗.每组10人,每人口服阿司匹林100 mg/d.通过活检提取受试者不同部位胃黏膜的总RNA和蛋白,采用RT/realtime PCR检测SLPI的mRNA表达水平和单抗ELISA定量测定SLPI蛋白,统计分析SLPI基因表达的相关数据.结果与Hp-组比较,Hp+组胃窦黏膜SLPI表达水平显著降低,但Hp+组经抗生素根除治疗后其SLPI水平恢复至与Hp-组相当的水平.在低剂量阿司匹林处理下,所有受试者表现组织学观察到的活动性或慢性炎性征.各组在药物处理的不同时间虽有一定的差异,但与药物处理对照组(第0天)比较,SLPI的表达差异没有统计学意义[第1天:(77±880)pg/10?g蛋白;第3天:(941±149)pg/10?g蛋白;第7天:(763±363)pg/10?g蛋白].阿司匹林处理的1周内以胃窦为主的胃炎持续存在(活动性:1.5～1.7;慢性:1.2～2.1),但与Hp-和Hpe(根除组)比较,Hp+组的胃窦黏膜SLPI蛋白表达仍显著降低.结论低剂量阿司匹林处理所致炎性反应对人胃黏膜SLPI的表达没有影响,胃窦黏膜SLPI基因表达的下调与Hp感染有关.

Objective To study the relationship between down-regulated expression of secretory leucocyte protease inhibtor in human gastric mucosa and Helicobacter pylori infection.Methods 20 volunteers were divialed into two groups. Oral administrations of aspirin were given to each subject in a dosage of 100 mg each day for one week. Biopsies of gastric and duodenal bulb mucosa from the subjects were collected. Proteins and mRNA of SLPI were respectively measured by quantitative ELISA and RT/real time PCR. Results In comparison with group Hp^- , level of SLPI expression of group Hp^＋ antral mucosa markedly declined to that of tip- group after eradication with antibiotics. In the treatment of low-dose, aspirin had inflammatory evidence. There were changes of SLPI expression at distinct time of the drug treatment among groups. However there was no statistical differences com- pared to control [day 1 ： （77 ± 880） pg/10 μg protein; day 3：（941± 149） pg/10μg protein; day 7：（763 μ 363） pg/10μprotein] though active and chronic gastrities were persistent during one week of aspirin treatment（ activity： 1.5-1.7, chronicity： 1.2-2.1）. Conclusion Inflammation resulted from low-dose aspirin treatment has no effect on SLPI expression in different Hp status. Down-regulation of SLPI expression of human antral mucosa results from Hp infection.