糖尿病大鼠脑中β-淀粉样蛋白变化的指标观察  

The Observation of Amyloid Beta Peptide in Diabetic Rat Brain

作　　者：王兴彬 曲忠森[2] 张清德[3] 孙保亮[4] 

机构地区：[1]山东省肥城市人民医院重症监护中心,271600 [2]上海交通大学附属第一人民医院神经科 [3]山东省菏泽医学专科学校内科学教研室 [4]山东省泰山医学院附属医院神经科

出　　处：《中国微循环》2007年第1期36-38,F0002,共4页Journal of Chinese Microcirculation

摘　　要：目的观察糖尿病(diabetes mellitus,DM)大鼠海马神经元β-淀粉样蛋白(amyloid betapeptide,Aβ)的变化。方法用链脲佐菌素(streptozotocin,STZ)建立DM大鼠模型,用32P放射性配体结合实验检测各组糖原合酶激酶-3(glycogen synthase kinase-3,GSK-3)的活性。用免疫组织化学的方法分别检测对照组、DM组、DM+Li2CO3组Aβ的表达。结果与对照组相比,DM组GSK-3的活性明显升高(P<0.01),Aβ表达明显增加(P<0.05),碳酸锂处理后GSK-3的活性明显降低(P<0.01),Aβ的表达下调(P<0.05)。结论DM大鼠海马GSK-3的活性异常增加,可能诱导Aβ的表达增加。Objective To investigate the alteration of Aβ peptide in diabetic rat hippocampus. Methotis The diabetic rats were induced by streptozotocin. The activity of glycogen synthase kinase-3 was measured by 32 P-labelling and the expression of Aβ was determined by immunohistochemistry in control group, DM group, DM ＋ Li2 CO3 group. Results The activity of GSK-3 was stimulated（P 〈 0.01）, the expression of Aβ was high（P 〈 0.05） in DM group. After the DM rats were treated with Li2 CO3, the activation of GSK-3 was decreased and the Aβ expression was reduced. Conclusion In DM rat brain, the activation of GSK-3 leads to overexpression of Aβ, and Li2 CO3 might reduce the expression of Aβ by inhibiting GSK-3.

关 键 词：糖尿病 糖原合酶激酶-3 碳酸锂 Β-淀粉样蛋白 

分 类 号：R587.1[医药卫生—内分泌]