脂联素降低tau蛋白的过度磷酸化水平
diponectin reduces hyperphosphorylation of tau protein
目的：分析脂联素对tau蛋白磷酸化程度的影响，并探讨其作用机制。方法：在小鼠脑神经瘤细胞 (Neuro-2a, N2a) 中，用RT-PCR的方法检测脂联素的两个受体AdipoR1/2 mRNA的表达，并用免疫印迹的方法检测所提脂联素的活性。用磷脂酰肌醇-3羟激酶 (phosphatidylinositol 3-hydroxy kinase，PI3K) 的抑制剂Wortmannin和蛋白激酶C (protein kinase C，PKC) 的抑制剂GF109203X联合加入到N2a细胞中，使tau蛋白异常过度磷酸化后，给予脂联素，观察tau蛋白的磷酸化水平变化；并用免疫印迹的方法检测Akt / GSK-3β通路的激活情况。 结果：（1）脂联素受体mRNA在N2a细胞中有表达，脂联素能在神经细胞中通过受体发挥生物学活性；（2）脂联素明显降低了tau蛋白的过度磷酸化水平。 结论：脂联素能降低tau蛋白过度磷酸化水平，这种作用主要通过Akt / GSK-3β通路来实现。
Objective: This paper explored the influence of adiponectin on the phosphorylation of tau and the possible mechanism. Methods: In Neuro-2a (N2a) cells, the expression of two adiponectin receptors mRNA were detected by RT-PCR. The activity of adiponectin was detected by Western blot. The PI3K inhibitor Wortmannin and the PKC inhibitor GF109203X were added into N2a cells, that induced tau hyperphosphorylation. Then, adiponectin was added into N2a cells, the level of tau phosphorylation was detected. Western blot detected the activity of Akt / GSK-3β pathway. Results: (1) The mRNA of AdipoR1 and AdipoR2 were expressed in N2a cells. Adiponectin could activate AMPK in N2a cells. (2) Adiponectin significantly reduced the level of tau phosphorylation. (3) Akt / GSK-3β pathway was involved in decreasing hyperphosphorylation of tau. Conclusions: Adiponectin can reduce the level of tau hyperphosphorylation by Akt / GSK-3β pathway.
张小曼、薛超、宋哲、尹君
基础医学神经病学、精神病学生物科学研究方法、生物科学研究技术
病理生理学，脂联素，tau蛋白，阿尔茨海默病，Akt，GSK-3β
Pathophysiology Adiponetin tau Alzheimer's disease Akt GSK-3β
张小曼,薛超,宋哲,尹君.脂联素降低tau蛋白的过度磷酸化水平[EB/OL].(2013-12-13)[2025-08-11].http://www.paper.edu.cn/releasepaper/content/201312-346.点此复制
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