Hutter-Paier B, Grygar E, Frühwirth M, Temmel I, Windisch M
Institute of Experimental Pharmacology, Research Initiative EBEWE, Graz, Austria.
J Neural Transm Suppl. 1998;53:363-72. doi: 10.1007/978-3-7091-6467-9_32.
The effects of Cerebrolysin on isolated chicken cortical neurons in an iron induced oxidative stress model and in a combined iron-glutamate model have been examined. In a first part of experiments it has been shown that under low serum conditions exposure of neurons to different concentrations of ammonium-iron (III)citrate (1, 5 microM AC-Fe3+) for 8 days caused a significant reduction in neuronal survival. Cerebrolysin not only prevented iron induced neurodegeneration, demonstrating that ionic iron was responsible for the cell damage, moreover, it increased the neuronal viability up to tenfold with respect to the controls. In the second part of the study neurons pre-incubated for 8 days with AC-Fe3+ were additionally lesioned with 1 mM L-glutamate and allowed to recover for another 48 h. Under these conditions cerebrolysin again clearly counteracted the in vitro destructive effects of glutamate. Besides consequences on the viability and survival of neurons Cerebrolysin increased abundance of the microtubule-associated protein MAP2, which is known to play a an important role in maintaining normal neuronal function.
已研究了脑蛋白水解物在铁诱导的氧化应激模型以及铁-谷氨酸联合模型中对离体鸡皮层神经元的影响。在实验的第一部分中，已表明在低血清条件下，将神经元暴露于不同浓度的柠檬酸铁铵（III）（1、5微摩尔AC-Fe3+）8天会导致神经元存活率显著降低。脑蛋白水解物不仅预防了铁诱导的神经变性，证明离子铁是细胞损伤的原因，此外，相对于对照组，它还使神经元活力提高了十倍。在研究的第二部分中，用AC-Fe3+预孵育8天的神经元再用1毫摩尔L-谷氨酸损伤，并使其再恢复48小时。在这些条件下，脑蛋白水解物再次明显抵消了谷氨酸的体外破坏作用。除了对神经元活力和存活的影响外，脑蛋白水解物还增加了微管相关蛋白MAP2的丰度，已知该蛋白在维持正常神经元功能中起重要作用。
