Moosavi Maryam, Maghsoudi Nader, Zahedi-Asl Saleh, Naghdi Nasser, Yousefpour Mitra, Trounce Ian Andrew
Department of Physiology, School of Medicine, Shahid Beheshti University, MC, Tehran, Iran.
Neuroendocrinology. 2008;88(4):293-8. doi: 10.1159/000150441. Epub 2008 Aug 1.
Corticosterone induces neuroanatomical and neurochemical changes in the hippocampus that are associated with cognitive impairments. In the present study corticosterone induced cell death in primary hippocampal neurons cultured in Neurobasal + B27 medium. Insulin prevents neuronal cell death induced in a concentration dependent manner. The neuroprotective effect of insulin was reversed by LY294002, a phosphatidylinositol 3'-kinase (PI3 kinase) inhibitor, whereas the mitogen-activated protein kinase (MAPK) inhibitor PD98059, an upstream blocker of MAPK had no effect. Western blot analyses showed that insulin induced the activation of protein kinase B (Akt). These results suggest that insulin can prevent neuronal cell death induced by corticosterone in hippocampal neurons by modulating the activity of the PI3 kinase/Akt pathway.
皮质酮会在海马体中引发与认知障碍相关的神经解剖学和神经化学变化。在本研究中，皮质酮在Neurobasal + B27培养基中培养的原代海马神经元中诱导细胞死亡。胰岛素以浓度依赖的方式预防神经元细胞死亡。磷脂酰肌醇3'-激酶（PI3激酶）抑制剂LY294002可逆转胰岛素的神经保护作用，而丝裂原活化蛋白激酶（MAPK）抑制剂PD98059（一种MAPK的上游阻断剂）则没有作用。蛋白质印迹分析表明，胰岛素可诱导蛋白激酶B（Akt）的激活。这些结果表明，胰岛素可通过调节PI3激酶/Akt信号通路的活性来预防皮质酮诱导的海马神经元细胞死亡。
