摘要
目的:观察急性损伤的胃黏膜雌激素诱导基因相关肽(TFF1)表达及应用泮托拉唑后的变化,探讨TFF1在应激胃黏膜损伤中的作用机制。方法:56只大鼠随机分为正常组、单纯造模组及造模干预组,各造模组制作大鼠水浸-束缚应激(WRS)模型,其中单纯造模组分为单纯造模1组(造模后即刻)、单纯造模2组(造模后4h)、单纯造模3组(造模后8h),造模干预组分为造模干预1组(造模后即刻)、造模干预2组(造模后4h)、造模干预3组(造模后8h),观察胃黏膜损伤指数(UI)及组织学变化,采用免疫组化法检测TFF1蛋白的表达。结果:水浸束缚应激后胃黏膜广泛损伤,单纯造模组UI升高,TFF1表达降低。予泮托拉唑干预后,与相应单纯造模组相比UI降低(单纯造模1组与造模干预1组69.13±1.97vs23.38±1.30,单纯造模2组与造模干预2组57.50±8.81vs10.38±3.02,单纯造模3组与造模干预3组43.50±6.76vs5.88±1.25,均P<0.01)。TFF1染色计分增加(单纯造模1组与造模干预1组0.55±0.11vs0.92±0.15,单纯造模2组与造模干预2组0.76±0.24vs1.36±0.21,单纯造模3组与造模干预3组1.12±0.16vs1.65±0.11,均P<0.01)。结论:TFF1可能参与胃黏膜保护,促进溃疡修复;泮托拉唑还可能通过上调雌激素诱导基因参与胃黏膜的防御屏障。
Objective: To investigate the effects of Pantoprazole on the expression of TFF1 in stress-induced gastric mucosal lesions in rats, and the mechanism thereof. Methods: Fifty-six rats were randomly divided into seven groups, normal group, model groups (3 groups) and model therapy groups (3 groups). The rat model of water immersionrestraint stress (WRS) was established in model groups, model group 1 (the immediately after establishing models), model group 2 (4 h after establishing models) and model group 3(8 h after establishing models). The model therapy groups were divided into model therapy group 1 (immediately after establishing models), model therapy group 2 (4 h after establishing models), and model therapy group 3 (8 h after establishing models). The ulcer index (UI) and histological changes were observed after WRS in rats. The expression of TFF1 was detected by immunohistochemistry. Results: After WRS, the gastric mucosa was widely damaged in rats. UI were increased and the expression of TFF1 was decreased in model groups. After intervention with Pantoprazole, UI was lower in model therapy group than those in model groups (model group 1 vs model therapy group 1,69.13±1.97 vs 23.38±1.30, P 〈 0.01; model group 2 vs model therapy group 2, 57.50±8.81 vs 10.38±3.02, P 〈 0.01; model group 3 vs model therapy group 3, 43.50±6.76 vs 5.88±1.25, P〈 0.01). The staining scores of TFF1 were increased (model group 1 vs model therapy group 1, 0.55±0.11 vs 0.92±0.15, P 〈 0.01; model group 2 vs model therapy group 2, 0.76±0.24 vs 1.36±0.21, P 〈 0.01; model group 3 vs model therapy group 3, 1.12±0.16 vs 1.65±0.11, P 〈 0.01). Conclusion: TFF1 may participate in the protection of gastric mucosa and promote ulcer recovery. Pantoprazole may participate in the defense of gastric mucosa through mediating the up-regulation of TFF1 expression.
出处
《天津医药》
CAS
北大核心
2009年第7期589-591,共3页
Tianjin Medical Journal
基金
天津市卫生局科技基金资助项目(项目编号:04KZ12)