幽门螺杆菌L型感染与食管癌及癌前病变中bcl-2表达关系的研究

目的研究幽门螺杆菌L型(HpL)感染对食管癌及癌前病变凋亡调节基因bcl2蛋白表达的影响,探讨Hp-L在食管癌发生发展过程中可能的致癌机制。方法应用免疫组化和革兰染色技术检测51例食管鳞状细胞癌(原位癌16例,浸润癌35例)及69例鳞状上皮增生性病变(单纯增生15例,轻、中、重度不典型增生分别为21例、18例、15例)和20例正常食管粘膜鳞状上皮组织中HpL型和bcl2蛋白的表达情况,对HpL型阳性和阴性组织的bcl2蛋白表达进行比较分析。结果不同组织类型HpL型检出率在中、重度不典型增生、原位癌、浸润癌均比较高(55.6%～62.9%),与正常组相比均有显著性差异(P<0.005)。在120例食管病变组织中,61例HpL型阳性者的bcl2蛋白表达阳性有48例,占78.7%;79例HpL型阴性者的bcl2蛋白表达阳性24例,占40.7%,两者比较有显著性差异(P<0.005)。各病变组中HpL型感染阳性组的bcl2蛋白表达阳性率高于HpL型阴性组的bcl2蛋白表达阳性率,其差异均有显著性(P<0.005～P<0.025)。表明HpL型感染与bcl2蛋白表达存在着相关性。结论HpL型可能通过影响bcl2蛋白表达,使食管粘膜上皮细胞凋亡调控异常而涉及食管癌的发生发展过程。

Relationship between Helicobacter Pylori L-form infection and the bcl-2 expression in esophageal cancer and precancerrous lesiors

To investigate the effects of Helicobacter Pylori L form(Hp L) infection on bcl 2 protein expression in esophageal cancer(EC),esophageal precancerrous lesiors(EPL) and the pathogenesis of EC.Hp L was examined in 51 patients with EC, 69 patients with EPL and 20 patients with normal esophageal mucosa(NEM) by Gram stain and immunohistochemical stain (ABC method) and bcl 2 protein were examined immunohistochemical stain (SP method).In different tissues, the positive rate of the Hp L infection in hyperplasia from mild to severe dysplasia lesions, carcinoma in situ and squsmous cell carcinomas of esophageal group were significantly higher than that in normal group with Gram stain and ABC method (55.6%～62.9%, P<0.005). In tissues of esophageal lesions of 120 cases,positive bcl 2 expression was found in 48 of 61 specimens of Hp L infection positive group(78.7%), and 24 of 79 specimens of Hp L infection negative group(40.7%). The expression of bcl 2 protein were significantly higher in esophageal lesions group than that in normal group, and the positive expression of bcl 2 in same esophageal lesions groups showed a significant correlation respectively(P<0.005). It showed that Hp L infection was correlated with the expression of bcl 2 protein in EC.It concluded that Hp L infection may affect expression of bcl 2 protein in EC, and thereby lead to increase of apoptosis in the epithelial cells of esophagus, therefore it act as a oncogenic agent in the occurrence and development of esophageal cancer.