摘要
目的通过研究幽门螺旋杆菌(HP)感染胃癌变过程中不同病理组织类型的环氧化酶2(COX-2)和p27kipl蛋白表达,探讨HP致癌的分子生物学机制。方法经胃镜和病理诊断明确的HP感染患者的不同胃粘膜组织标本共200例。包括慢性浅表性胃炎(CSG)、肠上皮化生(IM)、不典型增生(AH)、胃癌(GCA)各50例,分别以ABC和SP法测定COX-2和p27kipl蛋白表达情况。结果COX-2随癌变过程CSG→IM→AH→GCA的阳性率和表达强度不断提高,分别为12%、42%、52%、74%,GCA组与其它组相比,差异显著(P<0.05)。而p27kipl随癌变过程,CSG-IM-AH-GCA表达率逐步下降,分别为86%、46%、34%和26%,COX-2和p27kipl表达呈显著负相关。结论COX-2是HP感染胃癌变过程的早期事件,并参与了胃癌变的全过程,COX-2抑制了p27kipl的蛋白表达。
Objective To explore the molecular biological mechanism of cancerization in the different gastric pathologic tissue types after helicobacter pylori(HP) infection by studying the expres- sion of cyclooxygenase-2 (COX-2) and p27^kipl. Methods Two hundred samples of gastric mucous membrane were selected, which were taken from the patients definitely infected with HP diagnosed by gastroscope and pathology: chronic superfieal gastritis (CSG), intestinal metaplasia (IM), atypical hyperplasia(AH) and gastric carcinoma(GCA) with 50 specimens each. The expressions of COX-2 and p27^kipl were detected by ABC and SP respectively. Results Along with the development of cancerization,positive incidence and expression intensity of COX-2 increased gradually, which were 12%, 42 %, 52 % and 74 % for CSG, IM, AH and GCA respectively. The positive rate of COX-2 expression was significantly higher in group GCA than that in the other three groups(P〈0. 05). But the change of p27^kipl expression was opposite with the positive rates of 86 %, 46%, 34% and 26% for CSG, IM, AH and GCA respectively. There was a notable negative correlation between the expression of COX-2 and p27^kipl. Conclusion COX-2 is the early event during the course of gastric cancerization after HP infection and takes part in the total process. COX-2 inhibits the expression of p27^kipl.
出处
《江苏医药》
CAS
CSCD
北大核心
2005年第12期893-894,F0002,共3页
Jiangsu Medical Journal