摘要
目的 观察小鼠糖尿病脑淀粉样 β肽 (Aβ)和内质网Aβ结合蛋白 (ERAB)的变化 ,以了解糖尿病神经元退变的可能机制并观察淀粉样 β蛋白前体 (APP) 17肽的作用。 方法 用链脲佐菌素诱发糖尿病小鼠模型 ,并用APP17肽保护。 4周后 ,取脑 ,做APP17肽、Aβ 1～ 40、Aβ 1～ 42、Aβ 1～ 16及ERAB免疫组化染色。结果 正常小鼠海马内表达APP17肽、Aβ 1～ 40、Aβ 1～ 42、Aβ 1～ 16及ERAB的神经元数目少 ,染色淡 ,糖尿病小鼠海马内上述各种神经元的染色数目及染色程度均比正常小鼠明显增加 (P <0 .0 5 ) ,用APP17肽保护后 ,上述各种神经元染色数目及程度与正常小鼠接近。结论 糖尿病小鼠海马神经元表达Aβ和ERAB比正常小鼠明显增加 ,这可能是糖尿病脑病海马神经元退变的机制之一。APP17肽可使糖尿病小鼠Aβ及ERAB表达恢复正常 ,提示APP17肽有调节Aβ代谢和改善神经元退变的功能。
Objective To investigate the changes of amyloid β peptide (Aβ) and endoplasmic reticulum amyloid β peptide binding protein (ERAB) in the brain of diabetic mice, to understand the mechanism of neuron degeneration and to observe the effects of amyloid β protein precursor (APP)17 peptide on the foregoing changes. Methods Mouse diabetic model was induced by streptozotocin, and APP17 peptide was injected subcutaneously as a protective. Four weeks later, cryostat sections of mouse brain were prepared and immunohistochemically stained for APP17 peptide、 Aβ1～40、 Aβ1～42、 Aβ1～16 and ERAB. Results The number of neurons stained positively by antibodies of APP17 peptide、 Aβ1～40、 Aβ1～42、 Aβ1～16 and ERAB respectively in the hippocampus of brain in diabetic mice significantly increased as compared with normal controls (P<0.05). The result of APP17 peptide protected mice was the same as that in normal mice. Conclusion Compared with that of normal mice, neurons expressing Aβ1～42 and ERAB are significantly increased in number in the hippocampus of brain in diabetic mice (P<0.05), indicating that increased Aβ1～42 and ERAB is one of the important causes of neuronal degeneration in diabetic encephalopathy. APP17 peptide can normalize the expression of β amyloid peptide and its ERAB, indicating that APP17 peptide has regulatory effect on β amyloid peptide metabolism and retards neuron degeneration.
出处
《中华内分泌代谢杂志》
CSCD
北大核心
2000年第4期246-249,共4页
Chinese Journal of Endocrinology and Metabolism
基金
北京市科学技术委员会重点科技实验室基金资助项目!( 95 1890 60 0 )
