论文部分内容阅读
目的:探讨甲基苯丙胺 (methamphetamine, METH) 暴露引起的阿尔兹海默病 (Alzheimer's disease, AD) 样改变, 阐述L型钙通道在该病理样改变中的作用.方法:借助原代培养的神经元, 利用Western blot法, 观察METH (0、30、100、300、1 000μmol/L) 暴露后引起AD样病理性蛋白淀粉样蛋白前体 (amyloid precursor protein, APP) 、磷酸化Tau蛋白 (p-Tau) 的表达, 并观察钙通道抑制剂硝苯地平作用后APP、p-Tau表达的改变.结果:APP和p-Tau的表达随METH作用浓度和时间的增加而增高, 具有剂量和时间依赖性.钙通道抑制剂硝苯地平 (nifedipine, NIF) 预先孵育后, METH引起的AD样改变明显改善.结论:METH暴露可引起AD病理性改变, L型钙通道抑制剂可部分逆转上述改变, 因而L型钙通道可能作为对METH作用的干预靶点, 具有潜在的干预价值.“,”Objective:To investigate the Alzheimer disease (AD)-like changes caused by methamphetamine (METH) exposure, and to elucidate the role of L-type calcium channels in this pathological change. Methods:After primary cultured neurons were exposed to METH (0, 30, 100, 300, and 1 000 μmol/L), Western blotting assay was performed to investigate the expression of AD-like pathological protein amyloid precursor protein (APP) and p-Tau with or without the treatment of nifedipine. Results:After METH treatment, APP and p-Tau increased in a dose-dependent manner. Meanwhile, with a certain concentration of METH cultured with the neurons, the level of APP and p-Tau was increased in a time-dependent manner. After pre-incubation with the calcium channel inhibitor nifedipine (NIF), the METH-induced AD-like changes were significantly improved. Conclusion:METH exposure can cause AD pathological protein changes and L-type calcium channel ihhibitor can partially reverse the adverse changes, therefore, L-type calcium channel may be a potential intervention target for METH with the potential intervention value.