Leon A, Lipartiti M, Seren M S, Lazzaro A, Mazzari S, Koga T, Toffano G, Skaper S D
Fidia Research Laboratories, Abano Terme, Italy.
Stroke. 1990 Nov;21(11 Suppl):III95-7.
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. Systemic administration of GM1 appears to be efficacious in reducing acute neuronal damage and in facilitating medium- and long-term functional recovery after brain injury. We propose that GM1 protective effects in the acute injury phase results from attenuation of excitotoxicity, whereas the functional recovery seen at longer term could reflect GM1 potentiation of neuronotrophic factors. The potential therapeutic efficacy of GM1 administration in humans is suggested by clinical studies demonstrating improved neurologic outcome in stroke patients.
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，降低与兴奋性氨基酸相关的神经毒性。全身给予GM1似乎在减少急性神经元损伤以及促进脑损伤后的中长期功能恢复方面有效。我们提出，GM1在急性损伤期的保护作用源于兴奋性毒性的减弱，而长期观察到的功能恢复可能反映了GM1对神经营养因子的增强作用。临床研究表明中风患者的神经功能结局得到改善，提示了GM1在人类中的潜在治疗效果。
