COX-1、COX-2在小剂量阿司匹林相关性胃黏膜病变中的表达和意义

背景:阿司匹林系非甾体消炎药(NSAIDs)的代表药物,长期或过量服用可导致胃黏膜损伤。目前对于阿司匹林损伤胃黏膜的机制尚存在争议。目的:探讨环氧合酶(COX)-1、COX-2在阿司匹林相关性胃黏膜病变中的表达和意义。方法:选取2008年12月～2011年1月于清华大学第一附属医院诊断为小剂量阿司匹林相关性胃黏膜病变的患者136例,根据其胃镜下表现分为出血组、溃疡组、胃炎组,选取8例同期健康体检者作为正常对照组。应用免疫组化方法检测入选者胃黏膜组织中的COX-1、COX-2表达。结果:COX-1在正常对照组、胃炎组、溃疡组、出血组胃黏膜组织中的免疫组化评分(IHCS)逐渐降低,分别为7.75±3.62、1.76±1.05、1.33±0.79、1.08±0.65,各组间差异有统计学意义(P<0.05)。COX-2在正常对照组、胃炎组、溃疡组、出血组胃黏膜组织中的IHCS分别为7.50±3.34、7.30±2.15、7.28±2.72、7.33±3.17,各组间差异无统计学意义(P>0.05)。结论:小剂量阿司匹林是通过抑制COX-1途径而非COX-2途径导致胃黏膜损伤。

Expressions and Significance of COX-1 and COX-2 in Low-dose Aspirin Associated Gastric Mucosal Lesions

Background： Aspirin is one of the nonsteroidal anti-inflammatory drugs （NSAIDs） , however, long term use or large dose of aspirin is associated with gastric mucosal injury. Currently, the mechanism of aspirin-induced gastric mucosal injury is still a controversial issue. Aims： To study the expressions and significance of eyelooxygenase （COX） -1 and COX-2 in low-dose aspirin associated gastric mucosal lesions. Methods： A total of 136 patients with low-dose aspirin associated gastric mucosal lesions from Dec. 2008 to Jan. 2011 at First Hospital of Tsinghua University were enrolled in this study. According to the results of gastroscopy, patients were assigned into bleeding group, ulcer group and gastritis group. Eight healthy subjects were served as controls. Expressions of COX-1 and COX-2 in gastric mucosal tissue were determined by immunohistochemistry. Results： Immunohistochemistry score （IHCS） of COX-1 in control group, gastritis group, ulcer group and bleeding group were 7.75 ±3.62, 1.76 ± 1.05, 1.33 ± 0.79, and 1.08± 0.65, respectively. The differences between the four groups were statistically significant （P 〈 0.05 ）. IHCS of COX-2 in control group, gastritis group, ulcer group and bleeding group were 7.50± 3.34, 7.30 ± 2.15, 7.28 ± 2.72, and 7.33 ± 3.17, respectively. No significant differences were seen among the four groups （ P 〉 0.05 ）. Conclusions ： Low-dose aspirin induces gastric mucosal injury by inhibiting the COX-1 pathway rather than COX-2 pathway.