Department of Gastroenterology, Peking University First Hospital, Xicheng District, Beijing 100034, China.
Helicobacter. 2011 Feb;16(1):66-77. doi: 10.1111/j.1523-5378.2010.00811.x.
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.
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 PGE₂ was assessed by enzyme-linked immunosorbent assay.
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 PGE₂ 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 PGE₂ were detected in rats with esophageal H. pylori colonization.
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.
研究幽门螺杆菌（H. pylori）感染与 Barrett 食管（BE）的关系。建立慢性胃食管反流合并 H. pylori 感染的大鼠模型，评估炎症程度、BE 和食管腺癌（EA）的发生率。
将 8 周龄雄性无特定病原体（SPF）SD 大鼠随机分为 5 组：假手术组；食管空肠吻合术（EJA）组；EJA 合并 H. pylori 感染组；EJA 合并 H. pylori 感染和塞来昔布治疗组；EJA 合并塞来昔布治疗组。术后大鼠饲养 30 周。大体和显微镜下评估食管病变。通过 RT-PCR 和免疫组织化学染色检测 COX-2 和 CDX2 的表达。通过酶联免疫吸附试验评估 PGE₂水平。
EJA 合并 H. pylori 感染组大鼠食管黏膜损伤较 EJA 组减轻（p<0.05）。EJA 合并 H. pylori 感染组大鼠 BE 和 EA 的发生率高于 EJA 组，但无统计学差异。EJA 合并 H. pylori 感染大鼠给予塞来昔布治疗可降低 EA 的发生率（p<0.05）。与假手术组大鼠相比，H. pylori 感染或塞来昔布治疗大鼠的 CDX2 mRNA 表达降低（p<0.05）。与假手术组大鼠相比，EJA 大鼠无论是否合并 H. pylori 感染，COX-2 mRNA 表达和 PGE₂水平均升高（p<0.05），而给予塞来昔布治疗后则降低（p<0.05）。当 H. pylori 定植于食管时，炎症的严重程度、BE 和 EA 的发生率均显著增加。食管 H. pylori 定植大鼠 COX-2 表达和 PGE₂水平升高。
当 H. pylori 感染胃时，可能会减轻炎症的严重程度。然而，当定植于食管时，H. pylori 会增加食管炎症的严重程度和 BE、EA 的发生率。塞来昔布通过抑制 COX-2 表达减轻 EA 的发生率。
