Objective: To investigate the relation of cyclooxygenase-2(COX-2) expression with Helicobacter pylori (Hp)-associated gastroduodenal diseases, and to evaluate the effect of eradication of Hp infection on COX-2 expression in the antral mucosa of patients before and after antibiotic therapy. Methods: Tissues were obtained from 264 persons whose endoscopic and pathologic diagnoses were duodenal bulbar ulcer (DU, n=61),gastric ulcer(GU, n=63), compound ulcer (COU, n=28), gastric cancer (Gca, n=46), chronic gastritis (CG, n=55), normal (n=11) . 35 patients with chronic gastritis and Hp infection and subsequent eradication were studied.COX-2 protein was stained by immunohistochemical method. Gastritis, dysplasia, intestinal met-aplasia(IM) and Hp infection status were graded according to the updated Jinggangshan consensus of opinion. Results: In antral mucosa of all sections, patchy cytoplasmic staining of COX-2 protein could be detected on the surface and glandular epithelial cells, as well as lamina propria mesenchymal cells; but the vast majority of positively staining cells were seen on the surface epithelial region. The mean percentage of the cells staining with COX-2 was significantly higher in 143 Hp(+), in contrast with 110 Hp(-) (P=0).The similar statistical difference could be seen between Hp(+)and Hp(-)(P=0),and also seen in 27 patients between before and after successful eradication of Hp(P=0). However, compared with normal controls, the percentage of COX-2 expressing cells was significantly higher not only in the group of after successful eradication of Hp patients(P=0), but also in each group of Hp(-) patients(P<0.05).At the same time, compared with normal controls , COX-2 expressing levels had higher relation with the activity and degree of gastritis(P=0). In contrast with normal controls, in 75 patients with chronic active gastitis(CAG), and in 5 patients with dysplasia as well as in 13 patients with IM,COX-2 expression were significantly higher, and the dysplasia group was the highest.COX-2 immunostaining closely correlated with the degree of Hp(+)(rs=0.780, P=0)and the chronic inflammation score(rs=0.686, P=0). Conclusions: Hp infection leads to gastric mucosal overexpression of COX-2 protein, and COX-2 immunostaining closely correlated with the degree of Hp(+)and the chronic inflammation score; Despite the reduction in COX-2 expressions after Hp eradication , expression of COX-2 remained higher than normal control group. In Hp(-)CG and in IM as well as in dysplasia, COX-2 expressions were significantly higher than normal group; suggesting that the COX-2 is involved in both nonmalignant and malignant gastroduodenal diseases. |