Sun Wei-Hao, Yu Qian, Shen Hong, Ou Xi-Long, Cao Da-Zhong, Yu Ting, Qian Cheng, Zhu Feng, Sun Yun-Liang, Fu Xi-Ling, Su Han
Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China.
World J Gastroenterol. 2004 Oct 1;10(19):2809-13. doi: 10.3748/wjg.v10.i19.2809.
Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach.
Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining.
H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01).
COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.
环氧化酶(COX)-2在胃肠道肿瘤中过度表达。幽门螺杆菌(H pylori)感染与胃癌有因果关系。然而,COX-2在幽门螺杆菌相关胃癌发生途径各阶段的表达尚未阐明。因此,本研究的目的是阐明幽门螺杆菌诱导的COX-2表达在胃癌发生过程中的作用。
纳入138例受试者的胃活检组织(30例慢性浅表性胃炎(CSG)、28例胃腺体萎缩(GA)、45例胃黏膜肠化生(IM)、12例中度胃上皮发育异常和23例胃癌)。通过快速尿素酶试验和组织学检查(改良吉姆萨染色)评估幽门螺杆菌感染情况。采用免疫组织化学染色检测人胃黏膜中COX-1和COX-2的表达。
GA中幽门螺杆菌感染率为64.3%,胃癌中为69.5%,显著高于CSG中的感染率(36.7%)(P<0.05)。COX-2在CSG、GA、IM、发育异常和胃癌中的阳性表达率分别为10.0%、35.7%、37.8%、41.7%和69.5%。从CSG到GA、IM、发育异常,最后到胃癌,COX-2的表达呈上升趋势,而胃黏膜中COX-1的表达无明显变化。幽门螺杆菌阳性的IM和发育异常患者中COX-2的表达水平显著高于幽门螺杆菌阴性患者(P<0.01)。
幽门螺杆菌感染诱导的COX-2表达是胃癌发生过程中相对较早的事件。