幽门螺杆菌感染和环氧合酶-2表达在胃癌发生中的作用

The effects of Helicobacter pylori infection and cyclooxygenase-2 expression during the gastric carcinogenesis

目的 探讨幽门螺杆菌 (Hp)感染和环氧合酶 2 (COX 2 )表达在胃癌发生中的作用。方法 138例胃镜活检标本包括慢性非萎缩性胃炎 30例 ,慢性萎缩性胃炎 85例 (其中伴有中度以上肠化生 4 5例 ,中、重度异型增生 12例 ) ,和胃癌 2 3例。快速尿素酶试验和组织学改良Giemsa染色联合检测Hp ,免疫组化检查COX 1和COX 2表达。 结果 胃癌的Hp阳性率为 6 9.6 % ,显著高于慢性非萎缩性胃炎的 36 .7% (P <0 .0 5 )。慢性非萎缩性胃炎、慢性萎缩性胃炎、肠化生、异型增生和胃癌的COX 2表达率分别为 10 .0 %、37.6 %、37.8%、4 1.7%和 6 9.6 % ,而不同胃黏膜病变中COX 1表达无明显差异。慢性萎缩性胃炎、肠化生和异型增生中Hp阳性病例的COX 2表达显著高于Hp阴性病例 (P <0 .0 1)。 结论 Hp感染及其诱导的COX 2表达可能是胃癌发生的早期事件之一。

Objective To clarify the role of Helicobacter pylori (H. Pylori) that induced cyclooxygenase (COX)-2 expression during the gestric carcinogenesis. Methods A total of 138 gastric biopsies, including 30 cases with chronic non-atrophic gastritis, 85 cases with chronic atrophic gastritis (accompanying moderate or severe intestinal metaplasia 45 cases and dysplasia 12 cases), and 23 cases with gastric carcinoma were studied. H. pylori infection was assessed by rapid urease test and histological examination (modified Giemsa staining). Expression of COX-1 and COX-2 was detected by immunohistochemical stain. Results H. pylori infection rate was 69.6% in gastric carcinoma, significantly higher than 36.7% in chronic non-atrophic gastritis (P<0.05). The positive expression rates of COX-2 were 10.0%, 37.6%, 37.8%, 41.7% and 69.6% in chronic non-atrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric carcinoma respectively. From chronic non-atrophic gastritis to chronic atrophic gastritis to intestinal metaplasia to dysplasia to gastric carcinoma, expression of COX-2 showed as ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. COX-2 expression in chronic atrophic gastritis, intestinal metaplasia and dysplasia were significantly higher in H. pylori-positive than in H. pylori-negative subjects (P<0.01). Conclusion COX-2 expression induced by H. pylori infection is a relatively early event during carcinogenesis in the stomach.