急性胃粘膜损伤的机制研究

The Mechanism of Acute Gastric Mucosal Lesion

目的探讨胃粘膜细胞内还原型谷胱甘肽 (GSH)浓度与膜流动性及Na+ /K+ -ATP酶活力之间的关系。 方法将不同剂量的马来酸二乙酯 (DEM)溶解于 0 8ml花生油中给雄性Wistar大鼠作腹腔内注射 ,对照组注射等体积的花生油 ,30min后断颈处死动物 ,Guth法计算粘膜损伤指数 ,DNTB法测定粘膜内GSH浓度 ,紫外分光光度法测定Na+ /K+ -ATP酶活力 ,荧光分光光度法测定细胞膜流动性。 结果以不同浓度的DEM作腹腔注射后 ,胃粘膜损伤指数增加 ,粘膜内GSH呈剂量依赖性减少 ,Na+ /K+ -ATP酶活力下降 ,两者呈正相关 ,(r=0 8315 ,P <0 0 1)。 结论胃粘膜损伤与GSH含量下降。

Objective To study the correlation of glutathione (GSH) in the gastric mucosa with membrane fluidity and Na +/K +-ATPase activity. Methods Male Wistar rats were glutathione-depleted with different doses of diethylmaleate (DEM, 55 ～ 860mg/kg, i.p.). Each compound was dissolved in a constant volume (0.8ml) of arachidic oil and was given to the tested animal 30min before killing. Control animals received arachidic oil only. The index of the mucosal lesion was evaluated according to the Guth's method. The content of GSH was measured by the DNTB method. Na +/K +-ATP ase activity was determined by spectrophotometry. Membrane fluidity was assessed by the fluorescent polarization method. Results After administration of different doses of DEM, the gastric mucosal lesion index increased while there was a dose-dependent reduction in the GSH content and Na +/K +-ATPase activity. There was a positive relation ( r =0.8315, P <0 01). Conclusion GSH would be deple ted with DEM, while membrane fluidity and Na +/K +-ATPase activity declines. Thus a decrease in the GSH content and sodium pump dysfunction results in the gastric mucosal lesion.