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细胞外信号调节激酶在高血糖加重脑缺血性损伤中的作用

, PP. 133-136

Keywords: 细胞外信号调节激酶,高血糖,脑缺血,再灌注损伤

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Abstract:

探讨ERK1/2在高血糖加重大鼠脑缺血再灌注损伤中的作用。方法采用双侧颈总动脉管阻断加低血压法建立脑缺血再灌注模型,大鼠缺血前30min注射25%葡萄糖,使之处于高血糖状态。两侧颈总动脉结扎并放血,使血压下降到45~50mmHg。脑缺血30min后再灌注(解除颈总动脉结扎同时回输血液),分别观察再灌注后30min、1h、3h、6h。另设正常血糖组和对照组,用免疫组化和Westernblot比较3组大鼠ERK1/2的表达状态和脑组织病理改变。结果正常血糖组和高血糖组大鼠,再灌注后0~1h,海马CA1区未见明显的ERK1/2表达。而在纹状皮质和海马CA3区,ERK1/2的表达有明显的区别。正常血糖组大鼠在再灌后30min,可见ERK1/2轻度升高,高血糖组大鼠再灌注后30min,ERK1/2升高。ERK1/2在再灌注1h达到高峰并且持续到再灌注3、6h,高于正常血糖组(?P?<0?05)。用Westernblot方法检测皮质和海马的ERK1/2含量,正常血糖组在缺血再灌注30min、1h、3h、6hERK1/2含量逐渐升高,而高血糖组又高于正常血糖组(?P?<0?05)。结论高血糖可加重脑缺血再灌注损伤,其机制可能与激活ERK1/2有关。

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