β-内啡肽对谷氨酸神经毒性的增强作用。
Enhancing effects of beta-endorphin on glutamate neurotoxicity.
作者信息
Zhu L, Gao J, Wu J, Zhao X N, Zhang Z X
机构信息
School of Medicine, Nanjing University, China.
出版信息
Zhongguo Yao Li Xue Bao. 1998 Mar;19(2):108-11.
AIM
To study the effect of beta-endorphin (beta-End) on monosodium glutamate (MSG)-induced neurotoxicity (GNT).
METHODS
Image analysis of neuronal areas and determination of mitochondrial membrane protein-bound Ca2+ and intracellular free Ca2+ ([Ca2+]i) were used.
RESULTS
beta-End aggravated MSG-induced neuronal injury in arcuate nucleus of hypothalamus in a dose-dependent manner in the range from 0.5 to 5.0 mg.kg-1. MSG-induced increase in mitochondrial membrane protein-bound Ca2+ was enhanced when treated with beta-End 2 g.L-1. MSG-induced elevation in [Ca2+]i in single neuron was also augmented from 320 +/- 84 to 589 +/- 78 nmol.L-1 by the treatment with beta-End 2 g.L-1.
CONCLUSION
beta-End enhanced GNT via aggravating the disruption of intracellular Ca2+ homeostasis induced by MSG.
目的
研究β-内啡肽（β-End）对谷氨酸钠（MSG）诱导的神经毒性（GNT）的影响。
方法
采用神经元区域图像分析以及线粒体膜蛋白结合钙和细胞内游离钙（[Ca2+]i）的测定方法。
结果
在0.5至5.0mg.kg-1范围内，β-End以剂量依赖性方式加重了MSG诱导的下丘脑弓状核神经元损伤。当用2g.L-1的β-End处理时，MSG诱导的线粒体膜蛋白结合钙增加增强。用2g.L-1的β-End处理后，MSG诱导的单个神经元[Ca2+]i升高也从320±84增加到589±78nmol.L-1。
结论
β-End通过加重MSG诱导的细胞内钙稳态破坏来增强GNT。
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