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糖尿病小鼠脑组织超磷酸化及其机理研究 |
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赵咏梅 姬志娟 赵志炜 钱玉英 晋志高 裴进京 盛树力
【摘要】 目的 研究糖尿病小鼠脑内Tau蛋白是否过度磷酸化并观察APP17肽的作用。方法用链脲佐菌素诱发小鼠糖尿病模型，并皮下注射APP17肽对糖尿病小鼠进行保护。4周后，取脑组织做AT-8、Tau-1、PP-2B及用PP-2B脱磷酸后的Tau-1免疫组化染色。结果 糖尿病小鼠脑内AT-8阳性反应神经元数目多，胞浆和突起深染，而正常小鼠及APP17肽保护的糖尿病小鼠脑内阳性反应神经元数目少，染色淡；糖尿病小鼠海马内PP-2B阳性反应神经元数目比正常小鼠明显减少，用APP17肽保护后染色结果与正常小鼠接近。结论 糖尿病小鼠脑内出现Tau蛋白的过度磷酸化，即在丝氨酸202/苏氨酸205位点被磷酸化，PP-2B表达减少可能是导致Tau蛋白过度磷酸化的主要原因。用APP17肽可使PP-2B表达正常而保护Tau蛋白不被过度磷酸化。
【关键词】 糖尿病脑病 Tau蛋白 超磷酸化 小鼠
On the mechanism of Tau protein hyperphosphorylation
in brain tissues of diabetic mice
ZHAO Yongmei,JI Zhijuan,ZHAO Zhiwei,et al.
Beijing Research Laboratory for Brain Aging,Beijing Xuan Wu Hospital,Beijing,100053
【Abstract】 Objective To study whether Tau protein is hyperphosphorylated in brain tissues of diabetic mice and to study the effect of APP 17 peptide. Methods Mouse diabetic model was produced with streptozotocin, and APP 17 peptide as a protective was injected subcutaneously into diabetic mice. Four weeks later fixative was injected intravascularly into the mice, brain was removed and cryostat sections prepared. Immunohistochemical staining was done with AT-8, Tau-1, PP-2B antibodies, and again with Tau-1 antibody after dephosphorylation. Results In the brains of diabetic mice positive AT-8 reacting neurons were numerous, the cytoplasm was darkly stained, and 2-3 level dendritic processes were visible, while in normal mice and in APP 17 peptide-protected diabetic mice positive cells were scarce and were poorly stained. PP-2B enzyme was markedly diminished in the brains of diabetic mice in comparison to the controls. After APP 17 peptide protection positive staining of PP-2B approximated that in the controls. Conclusion Tau protein is hyperphosphorylated at Ser 202/Thr 205 sites in the brains of diabetic mice, which may be, chiefly due to reduction in PP-2B content. The use of APP 17 peptide can normalize the expression of PP-2B and protect Tau protein[1] [2] 下一页
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