胃癌及癌前病变幽门螺杆菌感染与Ki67、iNO表达关系

目的]探讨幽门螺杆菌(Hp)感染与Ki67、iNOS表达的关系,以及Hp感染导致胃癌形成的可能分子机制。方法]应用尿素酶试验和组织切片革兰染色检测115例胃黏膜组织的Hp;用免疫组化SP法检测上述组织的Ki67、iNOS表达,分析Ki67和iNOS及Hp感染三者之间的关系。结果]在正常黏膜、慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、腺癌组织中Hp检出率分别为0(0/8)、45.5%(5/11)、63.2%(12/19)、70.6%(12/17)、73.3%(11/15)、51.1%(23/45),病变各组中Ki67和iN-OS表达阳性率与浅表性胃炎组比较均有显著性差异(P<0.05)。除胃癌组外,病变各组的Ki67和iNOS的表达阳性率与各组的Hp感染阳性率呈正相关;每一病变组中Hp(+)组的Ki67和iNOS表达阳性率显著高于Hp(-)组,均有显著性差异(P<0.05)。结论]幽门螺杆菌感染与Ki67和iNOS阳性表达有一定的相关性,Hp可能通过促使细胞增殖加速和凋亡异常而涉及胃癌的发生过程。

Relationship Between Helicobacter Pylori and Expression of Ki67 and iNOS in Gastric Carcinoma and Pre-malignant Lesions

Purpose]To investigate relationship between expression of Ki67, iNOS(inducible nitric oxide synthase) and helicobacter pylori (Hp) infection as well as the possible oncogenetic molecular mechanism of Hp infection. Methods] Hp was detected in 115 cases with Hp-related gastric diseases by rapid urease test and Gram staining. Ki67 and iNOS were detected by immunohistochemical staining(SP method). Their relationship was analyzed. Results] The positive rates of Hp was 0 in normal gastric tissue, 45.5% in chronic superficial gastritis(CSG), 63.2% in chronic atrophic gastritis (CAG), 70.6% in intestinal metaplasia(IM), 73.3% in dysplasia(DYS), and 51.1% in gastric cancer(GC). Positive rates of Ki67 and iNOS between lesion group and superficial gastric group were significantly different(P<0.05). The positive rate of Hp in groups with lesions was positively correlated with the Ki67 and iNOS expressions except GC group. The positive rates of Ki67 and iNOS in Hp positive group were significantly higher than those in Hp negative group(P<0.05). Conclusion] Hp infection might induce proliferation and apoptosis of the gastric epithelial cells,these might lead to the occurrence of gastric cancer.