Effect of Helicobacter pylori Infection on Barrett's Esophagus and Esophageal Adenocarcinoma Formation in a Rat Model of Chronic Gastroesophageal Reflux
Effect of Helicobacter pylori Infection on Barrett's Esophagus and Esophageal Adenocarcinoma Formation in a Rat Model of Chronic Gastroesophageal Reflux
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DOI：
10.1111/j.1523-5378.2010.00811.x
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发表时间：
2011-02-01
期刊：
影响因子：
4.4
通讯作者：
Gao, Pei-Pei
中科院分区：
文献类型：
--
作者：
Liu, Fang-Xun;Wang, Wei-Hong;Gao, Pei-Pei
目的：为探讨幽门螺杆菌(Hp)感染与Barrett‘s食道(BE)的关系，建立慢性胃食道反流合并Hp感染的大鼠模型，观察其炎症程度、BE发生率和食管腺癌(EA)的发生率。方法：8周龄雄性SD大鼠随机分为5组：假手术组、食道空肠吻合组、E.A合并Hp感染组、EJA合并Hp感染+塞来昔布治疗组、EJA+塞来昔布治疗组。术后饲养30周。对食道病变进行大体和显微评价。逆转录-聚合酶链式反应和免疫组织化学染色检测COX-2和CDX2的表达。结果：EjA合并幽门螺杆菌感染组大鼠食道黏膜损伤程度明显低于EjA组(p<0.05)。幽门螺杆菌感染组大鼠的BE和EA发生率均高于对照组，但差异无统计学意义。塞来昔布治疗降低了幽门螺杆菌感染的大鼠的EA发生率(p<；0.05)。幽门螺杆菌感染组和塞来昔布治疗组大鼠CDX2基因的表达均低于假手术组(p<；0.05)。与假手术组相比，无论幽门螺杆菌感染与否，胃肠外营养组大鼠肺组织COX-2mRNA表达和PGE(2)水平均显著上调(p<；0.05)，塞来昔布治疗组大鼠COX-2mRNA表达和PGE(2)水平明显下调(p<；0.05)。当幽门螺杆菌定植于食道时，炎症程度及BE和EA的发生率显著增加。幽门螺杆菌定植大鼠胃组织中COX-2表达和PGE(2)水平升高。结论：幽门螺杆菌感染胃可能减轻炎症程度。然而，当幽门螺杆菌在食道定植时，会增加食管炎的严重程度和BE和EA的发生率。塞来昔布通过抑制COX-2的表达减少EA的发生。
Objectives:To investigate the relationship between Helicobacter pylori infection and Barrett's esophagus (BE), a rat model of chronic gastroesophageal reflux with H. pylori infection was established and the degree of inflammation, incidence of BE and esophageal adenocarcinoma (EA) were evaluated.Methods:Eight-week-old male specific-pathogen-free SD rats were divided into five groups randomly: pseudo-operation group; esophagojejunum anastomosis (EJA) group; EJA with H. pylori infection group; EJA with H. pylori infection and celecoxib-treated group; EJA with celecoxib-treated group. Rats were kept for 30 weeks after surgery. Esophageal lesion was evaluated grossly and microscopically. The expression of COX-2 and CDX2 was determined by RT-PCR and immunohistochemistry staining. The level of PGE(2) was assessed by enzyme-linked immunosorbent assay.Results:Esophageal mucosal injury in the group of EJA with H. pylori infection was decreased than that in EJA group (p < .05). The incidence of BE and EA in rats undergoing EJA with H. pylori infection was increased than in rats undergoing EJA with no statistical difference. Celecoxib treatment decreased the incidence of EA in rats undergoing EJA with H. pylori infection (p < .05). The expression of CDX2 mRNA was decreased in rats with H. pylori infection or treated with celecoxib than in the rats of pseudo-operation group (p < .05). When compared with those in rats of pseudo-operation group, the expression of COX-2 mRNA and the level of PGE(2) were upregulated in rats undergoing EJA irrespective of H. pylori infection (p < .05) and downregulated in rats treated with celecoxib (p < .05). When H. pylori colonized in esophagus, the severity of inflammation and the incidence of BE and EA were increased significantly. Higher levels of COX-2 expression and PGE(2) were detected in rats with esophageal H. pylori colonization.Conclusions:When H. pylori infect in stomach, it may reduce the severity of inflammation. However, when colonizes in esophagus, H. pylori increases the severity of esophageal inflammation and the incidence of BE and EA. Celecoxib administration attenuates the incidence of EA by inhibiting COX-2 expression.