摘要
蛋白磷酸酯酶（PP）－2A和一1的缺陷参与Alzheimer病（AD）微管相关蛋白tau的异常磷酸化，继而导致神经细胞退化死亡。本研究采用不同剂量PP－2A和PP－1的抑制剂Okadaicacid（以下简称OA）与成神经瘤细胞株（SH－SYSY）共培养，实验结果显示：OA导致细胞代谢明显降低，突起消失，微管受损，死亡加速。OA的上述细胞毒性在PP－2A和PP－1均被抑制时显著增强。该研究进一步为PP－2A和PP－1与神经细胞活性的关系提供了实验依据，也为建立AD蛋自磷酸酯酶缺陷实验模型奠定了基础。
It is well-known that the deficiency of protein phosphatases (PP)-1 and -2A is involved in abnormal pbosphorylation of microtubule-associated protein tau,and therefore,leading to neuronal degeneration in Alzheimer disease (AD). In the present study, different doses or pp-1 and PP-ZA specific inbibitor-okadaic acid (OA) were used in the culture medium of neuroblastoma cell line. The results show that the cells treated with OA have significantly decreased metabolism, dameged cell process and mlcrotubules,and increased cell death. An obvious lesion was round when both PP-1 and PP-2A were iuhlblted. As well as further demonstrate the involvement of PP-1 & PP-2A in neurofibrillary degeneration,the study has also provided new information for establishing cell models ror AD research.
