MCAO模型大鼠海马区1β-HSD1的表达及活性变化

目的探讨大鼠海马区11β-羟类固醇脱氢酶1（11β-HSD1）在局灶性脑缺血再灌注过程中的表达及活性变化。方法采用大脑中动脉线栓法（MCAO）建立大鼠局灶性脑缺血-再灌注模型。42只雄性SD大鼠，随机分为脑缺血-再灌注后4、8、12、24、48、72h组和假手术组，每组6只。采用核糖核酸酶保护实验检测11β-HSD1mRNA的表达，采用Westernblot方法分析11β—HSD1蛋白表达水平变化，采用薄层层析（TLC）方法检测11β-HSD1酶活性。结果短暂性脑缺血-再灌注后大鼠海马区11β－HSD1表达增强，并于再灌注后24h达高峰，且11β-HSD1酶的活性也呈现类似变化规律。结论海马区11β—HSD1表达和活性的异常可能参与了大鼠脑缺血-再灌注损伤的病理生理过程。

Expression and activities of 11beta-hydroxysteroid dehydrogenase type 1 in rat hippocampus after middle cerebral artery occlusion

Objective To investigate the expression and activities of llbeta-hydroxysteroid dehydrogenase type 1 （11β-HSD1） in rat hippocampus after focal cerebral ischemia-repeffusion. Methods The focal cerebral ischemia-reperfusion model was induced in rats by thread embolism of middle cerebral artery. Forty-two male SD rats were randomly divided into sham-operation group and groups of 4 h, 8 h, 12 h, 24 h, 48 h and 72 h after focal cerebral ischemia-repeffusion. Ribonuclease protection assay and Western blotting were used to detect 11β-HSD1 mRNA and protein expression. Thin-layer chromatography （TLC） were used to analyze the activities of 11β-HSD1. Results Both mRNA and protein expression of 11β-HSD1 at 8 h, 12 h, 24 h, 48 h, 72 h after reperfusion were up-regulated cotrqoared to the sham operation group （P〈0.05）, and reached the peak at 24 h after reperfusion. The activities of 11β-HSD1 enzyme also showed the similar changes. Conclusion Changes of 11β-HSD1 expression and activity in rat hippocampus way be involved in the pathophysiological process of cerebral ischemia-reperfusion injury.