K. Jovanova-Nešić, M. Eric-Jovicic, M. Popovic, N. Popovic, L. Rakić, N. H. Spector
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引用次数: 2
Abstract
In a previous paper, the authors (1997) have described the effect of Ca/sup 2+/-antagonist verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD). The present paper is concerned with the effect of magnetic stimulation of pineal complex on Na,K-ATPase activity in the same experimental model of AD. Since accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter free radicals reactions, we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na,K-ATPase activity. Results are presented as Vmax/Km parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac function. Stimulation of pineal complex of the brain more than ten days, by magnetic beads (600-Gauss flux density) fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na,K-ATPase activity. Results are presented as Vmax/Km parameters on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. These results confirm the hypothesis that altered ion homeostasis disturbed by neuro-degenerations play an essential role in pathogenesis of experimental AD and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na,K-ATPase activity.
在之前的论文中,作者(1997)描述了Ca/sup 2+/-拮抗剂维拉帕米对阿尔茨海默病(AD)实验模型中Na, k - atp酶的影响。本文研究了磁场刺激松果体复合体对AD实验模型中Na, k - atp酶活性的影响。由于积累的数据表明自由基介导AD中神经元的损伤和死亡,并且由于磁场(MFs)可以改变自由基反应,我们验证了静止的MFs通过膜Na, k - atp酶活性介导离子稳态的假设。结果为大细胞基底核损伤大鼠外周血红细胞膜Vmax/Km参数。双侧电解或kainic酸诱导的NBM病变导致心功能获得的红细胞膜Vmax/Km活性显著降低。刺激大脑松果体复合体十天以上,通过磁珠(600高斯磁密度)固定在颅骨上的松果体上,明显增加受损病变的NBM、Na、k - atp酶活性。结果为基底前脑束NBM损伤大鼠外周血红细胞膜Vmax/Km参数。这些结果证实了由神经变性引起的离子稳态改变在实验性AD发病机制中起重要作用的假设,并且松果体复合体的磁刺激可能成功恢复受神经元死亡干扰的Na, k - atp酶活性。