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神经节苷脂GM1可诱导大鼠克隆性嗜铬细胞瘤细胞系PC12h中B型单胺氧化酶的表达。

Ganglioside GM1 causes expression of type B monoamine oxidase in a rat clonal pheochromocytoma cell line, PC12h.

作者信息

Naoi M, Suzuki H, Takahashi T, Shibahara K, Nagatsu T

机构信息

Department of Biochemistry, Nagoya University School of Medicine, Japan.

出版信息

J Neurochem. 1987 Nov;49(5):1602-5. doi: 10.1111/j.1471-4159.1987.tb01033.x.

Abstract

The effects of ganglioside supplementation of culture medium on monoamine oxidase (MAO) type A and B activities in a rat clonal pheochromocytoma cell line, PC12h, were examined. The MAO activity in PC12h cells proved to be mainly due to type A MAO, and type B MAO activity was negligible. After supplementation of the culture medium with ganglioside GM1, the PC12 cells were found to express type B MAO activity after 4 days of culture, and the amount of type B activity increased with the number of days of culture. After 3 weeks of culture in the presence of GM1, type B activity was about 10% of the total, whereas in control cells type B MAO activity was only about 0.6% of the total. By kinetic analyses of type A and B MAO in PC12h cells after 3 weeks of culture, the increase of type B MAO activity was found to be due to the increase in amount of type B MAO; the Km values were almost the same and only the Vmax values were increased in the cells supplemented with GM1. Among gangliosides tested GM1 was the most effective in causing expression of type B MAO activity, whereas nerve growth factor was not effective. These results suggest that GM1 and other gangliosides may be involved in the expression of type B MAO in nerve cells and in the regulation of levels of the biogenic amines in the brain.

摘要

研究了在大鼠克隆嗜铬细胞瘤细胞系PC12h的培养基中添加神经节苷脂对A型和B型单胺氧化酶(MAO)活性的影响。结果表明,PC12h细胞中的MAO活性主要归因于A型MAO,B型MAO活性可忽略不计。在培养基中添加神经节苷脂GM1后,发现PC12细胞在培养4天后表达B型MAO活性,且B型活性的量随培养天数增加。在GM1存在下培养3周后,B型活性约占总量的10%,而在对照细胞中,B型MAO活性仅约占总量的0.6%。通过对培养3周后的PC12h细胞中的A型和B型MAO进行动力学分析,发现B型MAO活性的增加是由于B型MAO量的增加;在添加GM1的细胞中,Km值几乎相同,只有Vmax值增加。在所测试的神经节苷脂中,GM1在引起B型MAO活性表达方面最有效,而神经生长因子则无效。这些结果表明,GM1和其他神经节苷脂可能参与神经细胞中B型MAO的表达以及大脑中生物胺水平的调节。

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