目的　研究选择性环氧合酶 2抑制剂对化学诱导胃溃疡形成和愈合的影响 ,同时探讨其可能机制。方法　雄性SD大鼠 ,体重 16 0～ 180g。分两组 ,即单纯乙酸诱导胃溃疡作为对照组和乙酸诱导胃溃疡加NS 398处理组 ,各时间点每组均 8只。乙酸诱导胃溃疡后 1、3和 7d用RT PCR和Westernblot分别检测胃粘膜中环氧合酶 2 (COX 2 )和诱导型一氧化氮合酶的表达。用ELISA测定胃粘膜中前列腺素E2 (PGE2 )量反映COX活性。同时研究选择性COX 2抑制剂NS398对iNOS表达、活性及胃粘膜损伤的影响 ,以溃疡面积来评估胃粘膜损伤程度。结果　RT PCR结果显示乙酸诱导大鼠胃溃疡后 ,COX 2mRNA表达明显升高 ;以溃疡基底部为明显。胃粘膜PGE2 合成也明显增高。NS 398能抑制胃粘膜PGE2 的合成 ,溃疡诱导后 1d处理组溃疡面积小于对照组 ,且周围充血水肿较轻 ;3d时两组溃疡大小无差异 ;但 7d时NS 398组溃疡面积大于对照。同时NS 398能降低胃粘膜iNOS的表达及活性。结论　抑制COX 2活性能减轻溃疡形成初期炎症反应 ,使组织免受进一步损伤 ,但延缓溃疡愈合。这一作用除和PGE2 合成减少有关外 ,可能尚和抑制iNOS表达和活性有关。 Objective To investigate the effects of selective cyclooxygenase 2 inhibitors on the formation and healing of chemically induced gastric ulcer, and to explore its possible mechanism. Methods Male SD rats weighing 16 0 ~ 180g. Divided into two groups, namely simple acetic acid-induced gastric ulcer as a control group and acetic acid-induced gastric ulcer plus NS 398 treatment group, each time point of each group of 8. The expression of cyclooxygenase 2 (COX 2) and inducible nitric oxide synthase in gastric mucosa were detected by RT PCR and Western blot at 1, 3 and 7 days after acetic acid induced gastric ulcer. The amount of prostaglandin E2 (PGE2) in the gastric mucosa was measured by ELISA reflecting COX activity. At the same time study the selective COX 2 inhibitor NS398 on iNOS expression, activity and gastric mucosal injury, ulcer area to assess the degree of gastric mucosal injury. Results RT-PCR results showed that the expression of COX-2 mRNA in gastric ulcer induced by acetic acid was significantly increased, and the basal part of ulcer was obvious. Gastric mucosal PGE2 synthesis was also significantly higher. NS 398 could inhibit the gastric mucosal PGE2 synthesis. After ulcer induction, the ulcer area of ​​the treated group was smaller than that of the control group, and the congestion and edema around the lesion was mild. There was no difference in the ulcer size between the two groups. At the same time NS 398 can reduce gastric mucosal iNOS expression and activity. Conclusion Inhibition of COX 2 activity can reduce the initial inflammatory reaction in ulcer formation and prevent the tissue from further damage, but delay the healing of ulcer. In addition to the role of PGE2 synthesis and reduce the relevant, may inhibit the iNOS expression and activity.