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MPP+和6-OHDA是两种广泛用于构建帕金森疾病动物和细胞实验模型的神经毒素.许多研究表明:parkin蛋白功能异常是帕金森疾病发生的主要原因.前期研究发现,MPP+和6-OHDA处理SH-SY5Y神经细胞能诱导线粒体破碎,并且parkin蛋白表达下降,然而线粒体破碎是否与parkin减少有关,目前还不是很清楚.本研究发现MPP+和6-OHDA均能引起parkin的底物蛋白Drp1水平增加,而Drp1参与调控线粒体的分裂,线粒体分裂过度会破碎成点状.在parkin敲除的成纤维细胞内也发现线粒体破碎的现象,外源表达parkin质粒可以恢复线粒体的形态,从而证实MPP+和6-OHDA诱导线粒体破碎与parkin/Drp1有关.
MPP + and 6-OHDA are two neurotoxins that are widely used in animal and cell model of Parkinson’s disease.Many studies have shown that: Parkin protein dysfunction is the main cause of Parkinson’s disease.Previous studies found that MPP + and 6-OHDA Treatment of SH-SY5Y neurons induced mitochondrial fragmentation and decreased expression of parkin protein, however, whether mitochondrial fragmentation is associated with a decrease in parkin is still unclear.We found that both MPP + and 6-OHDA can cause Parkin protein levels of Drp1 And Drp1 involved in the regulation of mitochondrial division, mitochondrial overgrowth will break into dots in the parkin knockout fibroblasts also found mitochondrial fragmentation phenomenon, exogenous expression of parkin plasmid can restore mitochondrial morphology, thus confirming the MPP + and 6-OHDA-induced mitochondrial fragmentation is associated with parkin / Drp1.