目的 观察硫化氢供体硫氢化钠(NaHS)预处理对大鼠水浸束缚所致胃黏膜损伤的影响,并对其机制进行探讨.方法 SD大鼠分为正常组、水浸束缚组(WRS组)及NaHS预处理组.NaHS预处理组大鼠腹腔连续注射NaHS(10 μmol·kg-1·d-1) 7、14、21天后水浸束缚6 h.计算大鼠水浸束缚后胃黏膜大体损伤面积,免疫印迹方法检测胃黏膜组织黄嘌呤氧化酶(XOD)和超氧化物歧化酶(SOD)的表达.结果 WRS组大鼠胃黏膜损伤面积明显高于正常组;NaHS预处理7、14、21天能够减少水浸束缚引起的胃黏膜损伤面积(P<0.05);与WRS组比较,NaHS预处理各组的XOD表达下降(P<0.05)、SOD表达升高(P<0.05).结论 NaHS预处理对水浸束缚大鼠胃黏膜损伤具有保护作用,推测其机制是硫化氢通过提高胃黏膜组织SOD活性、减少XOD表达,促进机体清除氧自由基,同时减少氧自由基生成,从而减轻水浸束缚对胃黏膜的损害作用.%Objective To investigate the protective effect of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by water-immersion restraint stress in rats. Methods SD rats were divided into contral group, WRS group and NaHS pretreatment groups . Gastric injury induced in rats by 6 h of water immersion and restraint stress (WRS) was determined after NaHS pretreatment for 7,14 and 21 days. Gastric mucosal damage was analyzed with macroscopic injured area. The contents of XOD and SOD were measured by Western blot . Results Compared to control group, the injured area of gastric mucosa induced by water-immersion restraint stress increased. Pretreatment of NaHS significantly reduced the injured area of the gastric mucosa induced by WRS (P<0.05). The increases of XOD and decreases of SOD in WRS group were significantly inhibited by NaHS pretreatment (P<0.05) . Conclusion These results suggest that exogenous hydrogen sulfide exerts a protective action on the gastric mucosa of rats exposed to water-immersion restraint stress possibly through increasing SOD activity , decreasing XOD expression and oxygen free radical overpro-duction.
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