Kolobov V V, Zakharova I A, Fomina V G, Gorbatov V Yu, Davydova T V
Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russia.
Bull Exp Biol Med. 2013 Feb;154(4):425-7. doi: 10.1007/s10517-013-1967-x.
Experiments on rats have showed that neurodegenerative damage to the brain induced by injection of a neurotoxic β-amyloid protein fragment β25-35into the basal giant cell nuclei of Meynert activated caspase-3 in the prefrontal cortex and hippocampus on day 3 after injury. Intranasal administration of antibodies to glutamate in a dose of 300 μ g/kg 1 h after damage reduced enzyme activity in these structures in a rat model of Alzheimer's disease.
对大鼠的实验表明，通过向Meynert基底巨细胞核注射神经毒性β-淀粉样蛋白片段β25-35诱导的大脑神经退行性损伤，在损伤后第3天激活了前额叶皮质和海马体中的半胱天冬酶-3。在阿尔茨海默病大鼠模型中，损伤后1小时以300μg/kg的剂量鼻内给予谷氨酸抗体可降低这些结构中的酶活性。
