Carolei A, Fieschi C, Bruno R, Toffano G
Istituto di Scienze Neurologiche, Università degli Studi di Siena, Italy.
Cerebrovasc Brain Metab Rev. 1991 Summer;3(2):134-57.
In vitro studies have shown that monosialoganglioside GM1 reduces excitatory amino acid-related neurotoxicity by limiting the downstream consequences of abusive excitatory amino acid receptor stimulation, while enhancing neuronotrophic factor action in a variety of neuronal cell types. Systemic administration of GM1 appears to be efficacious in reducing acute nerve cell damage and in facilitating medium- and long-term functional recovery after brain injury. Although the mechanism of action remains unclear, it appears likely that GM1 protective effects in the acute injury phase are at least in part due to the attenuation of excitotoxicity, while the long-term functional recovery might reflect GM1 potentiation of neuronotrophic factors. The potential therapeutic efficacy of GM1 administration in different conditions in humans, as suggested by pioneer clinical studies, is reviewed. Further larger, randomized, double-blind clinical studies are necessary to define the therapeutic efficacy.
体外研究表明，单唾液酸神经节苷脂GM1通过限制过度刺激兴奋性氨基酸受体的下游后果，降低兴奋性氨基酸相关的神经毒性，同时增强多种神经元细胞类型中神经营养因子的作用。GM1的全身给药似乎在减少急性神经细胞损伤以及促进脑损伤后的中长期功能恢复方面有效。尽管作用机制尚不清楚，但GM1在急性损伤期的保护作用似乎至少部分归因于兴奋性毒性的减弱，而长期功能恢复可能反映了GM1对神经营养因子的增强作用。本文综述了早期临床研究所提示的GM1给药在人类不同情况下的潜在治疗效果。需要进一步开展更大规模的随机双盲临床研究来确定其治疗效果。
