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背景胃黏膜诱生型一氧化氮合酶(iNOS)的过度表达在应激性溃疡的发生中起重要作用。目的研究褪黑激素(MT)对水浸鄄束缚应激大鼠胃黏膜iNOS表达的影响及其对胃黏膜的保护作用,以进一步阐明MT的作用机制。方法正常对照组不予水浸鄄束缚应激和MT预防,模型组和MT低剂量预防组、MT高剂量预防组于应激前30min分别腹腔注射含1%二甲基亚砜(DMSO)或MT5mg/kg、20mg/kg的等体积生理盐水。应激6h后处死动物,检测各组大鼠胃黏膜一氧化氮(NO)水平、iNOS蛋白和iNOSmRNA的表达,并评估胃黏膜损伤程度。结果水浸鄄束缚应激6h后,大鼠胃黏膜NO水平、iNOS蛋白和iNOSmRNA表达显著增加,胃黏膜病变明显。MT预防组大鼠胃黏膜NO水平、iNOS蛋白和iNOSmRNA表达均显著低于模型组(P<0.01),且溃疡指数(UI)显著下降(P<0.01)。MT高剂量预防组大鼠各检测指标均显著低于MT低剂量预防组(P<0.05),作用呈剂量依赖性。结论MT可预防水浸鄄束缚应激诱导的大鼠胃黏膜损伤,其机制可能与其抑制胃黏膜iNOS过度表达有关。
Background Overexpression of gastric inducible nitric oxide synthase (iNOS) plays an important role in the development of stress ulcer. Objective To study the effect of melatonin (MT) on iNOS expression in gastric mucosa and its protective effect on gastric mucosa in water-immersion restraint stress-induced stress rats, so as to further elucidate the mechanism of action of MT. Methods Normal control group was given no water immersion and restraint stress and MT prophylaxis. The model group and MT low dose prevention group and MT high dose prophylaxis group were intraperitoneally injected with DMSO containing 1% DMSO or MT5mg / kg, 20mg / kg of equal volume of normal saline. The animals were sacrificed 6h after stress. The levels of nitric oxide (NO), iNOS protein and iNOS mRNA in gastric mucosa of rats in each group were measured, and the degree of gastric mucosal damage was evaluated. Results After 6 h immersion-restraint stress, the gastric mucosal NO level, iNOS protein and iNOS mRNA expression were significantly increased, and gastric mucosal lesions were obvious. The gastric mucosal NO level, iNOS protein and iNOS mRNA expression in MT-treated group were significantly lower than those in model group (P <0.01), and the ulcer index (UI) decreased significantly (P <0.01). MT detection of high-dose group of rats were significantly lower than the detection of low-dose MT prevention group (P <0.05), the role of a dose-dependent manner. Conclusion MT can prevent water-trap-induced stress-induced gastric mucosal injury in rats, and its mechanism may be related to its inhibition of gastric mucosal iNOS overexpression.