摘要
目的:探讨反流致大鼠Barrett s食管(Barrett se sophagus,BE)及食管腺癌(esophagealadenocarcinoma,EAC)发 生过程中局部诱导型一氧化氮合酶(iNOS)的表达及意义. 方法:将8wk龄雄性SD大鼠65只,通过手术建立十二指肠 胃食管反流模型组,分别于术后1,4,8,12,16,20wk随机取 若干动物食管全长,制成纵切面石蜡切片,分别进行苏木精 伊红(HE)染色及iNOS免疫组化染色,在光镜下观察食管黏 膜病变及iNOS染色结果.另设无反流对照组(10只).结果: ①对照组未见病变;模型组术后引发反流性食管炎,食管下 段黏膜炎症和增生的程度随观察时间的延长逐渐加重,并有 部分发展为BE和起源于BE的EAC.BE、EAC最早分别出现 于术后第8周和第12周,在以后的各时间点两者发生率呈上 升趋势,到术后20wk达86.6%和53.3%.②对照组iNOS阴 性.模型组术后1,4,8,12,16。
AIM: To investigate the expression and significance of inducible nitric oxide synthase (iNOS) in the formation of Barrett's esophagus (BE) and its progression to esophageal adenocarcinoma (EAC) in a rat model. METHODS: Sixty-five eight-week-old male Sprague-Dawley rats underwent end-to-side gastrojejunostomy, followed by end-to-side esophagojejunostomy approximately 0.5 cm distal to the gastro-jejunostoma to produce the duodenogastroesophageal reflux model group. Another 10 rats undergoing a sham operative procedure were taken as a control group. Some animals were sacrificed and their esophageal samples were taken from the model group at week 1, 4, 8, 12, 16 and 20 respectively after surgery and from the control group at week 20. Longitudinally esophageal paraffin slides were made and used for hematoxylin and eosin staining and iNOS immunohistochemical staining. Pathological changes and expression of iNOS in the distal one-third of the esophageal mucosa were detected microscopically. RESULTS: ① No pathological changes were found in the control group. Significant esophagitis were observed in the model group after surgery. There was a progression in epithelial cell proliferation and inflammation from mild to severe in the distal one-third of the esophagus, and BE and EAC were observed. The incidence of BE and EAC increased with time: 37.5% and 0% at week 8, 60% and 10% at week 12, 90% and 30% at week 16, 86.6% and 53.3% at week 20. ② Immunohistochemical staining of iNOS was negative in the control group. In the model group positive expression of iNOS in the distal one-third of the esophagus was observed in 0%, 0%, 50%, 80%, 100% and 100% of the rats at week 1, 4, 8, 12, 16 and 20 respectively and in 100% of the rats with BE and EAC. Positive iNOS staining was observed in the stromal macrophages directly beneath the epithelium. CONCLUSION: Excessive nitric oxide produced by iNOS in the stromal macrophages may contribute to the pathogenesis of BE and its progression to EAC.
出处
《第四军医大学学报》
北大核心
2005年第2期150-153,共4页
Journal of the Fourth Military Medical University
