根除幽门螺杆菌对胃黏膜萎缩并肠上皮化生以及COX-2、C- met表达的影响

目的研究幽门螺杆菌(helicobacter pylori,Hp)根除前后胃黏膜萎缩和肠上皮化生的变化以及环氧合酶-2(cyclooxygenase-2,COX-2)和肝细胞生长因子受体(C-met)的表达。方法 13例患者均为胃镜加病理确诊有萎缩并肠化生合并HP感染,且成功根除HP感染者。用免疫组化方法半定量检测HP除前后萎缩性胃炎并肠上皮化生COX-2蛋白和C-met蛋白的表达。结果根除前和根除后1个月萎缩程度积分分别为1.3±0.3,1.2±0.7,根除后1个月与根除前比较无显著差异(P>0.05)。萎缩并肠化生胃黏膜C-met平均阳性细胞率从根除前53.2±12.4％下降至根除后48.8±7.7％,比较有显著差异(P=0.034)。胃黏膜COX-2平均阳性细胞率从根除前36.5±14.0％下降至根除后23.3±7.9％,有显著差异(P=0.023)。COX-2表达与C-met表达有一定的相关性(r=0.310,P<0.05)。结论 HP根除短期内不能逆转胃黏膜萎缩,但可使慢性萎缩性胃炎胃黏膜中COX-2和C-met癌基因表达下降。COX-2表达与C-met表达相关。

Effect of Helicobacter pylori eradication on COX-2 and C-met expression atrophy with intestinal metaplasia in gastric mucosa

Objective To investigate COX-2 and C-met expression and the change of atrophy with intestinal metaplasia in gastric mucosa before and after eradication of Helicobacter pylori (HP). Methods Tissues were obtained from patients with gastric atrophy and intestinal metaplasia undergoing HP treatment. COX-2 and C-met protein were stained by immunohistochemieal method. Results Atrophy and intestinal metaplasia did not change before and after eradication of Helicobacter pylori. COX-2 expression in gastric atrophy and intestinal metaplasia mucosa with HP infection was significantly higher when compared with that after successful HP eradication (P<0.05). C-met expression in gastric atrophy and intestinal metaplasia mucosa with HP infection was significantly higher when compared with that after successful HP eradication (P<0.05), COX-2 and C-met expression in gastric atrophy and intestinal metaplasia mucosa with HP infection was not significantly changed when compared with that non-successful HP eradication (P>0.05). COX-2 expression was significantly correlated with C-met expression (r=0.310, P<0.05). Conclusions Eradication of HP in short term can not change atrophy, but it can improve COX-2 and C-met expression in gastric preneoplassitc lesion, and COX-2 expression was significantly correlated with C-met expression, suggesting that COX-2 with expression of oncogene is involved in formation of HP-related early gastric carcinoma.