Sato H, Hariyama H, Moriguchi K
Research Laboratories, Fuji Chemical Industry Co., Ltd., Toyama, Japan.
Biochem Biophys Res Commun. 1988 Jan 15;150(1):491-6. doi: 10.1016/0006-291x(88)90547-5.
We investigated the effect of S-adenosyl-L-methionine (SAMe) on the prevention of the delayed neuronal death in rats subjected to transient and brief forebrain ischemia. As the results, SAMe dose-dependently protected the hippocampal CA1 neurons from degeneration and necrosis, whose effect was suppressed by simultaneous administration of S-adenosyl-L-homocysteine, a potent inhibitor in transmethylation. No protective effect was observed in CDP-choline, phosphatidylcholine and L-methionine. Therefore, it is necessary for the prevention of the delayed neuronal death to enhance cerebral SAMe level and to activate transmethylation using SAMe as a methyl donor in postischemic brain.
我们研究了S-腺苷-L-甲硫氨酸(SAMe)对短暂性和短暂性前脑缺血大鼠延迟性神经元死亡的预防作用。结果显示,SAMe剂量依赖性地保护海马CA1神经元免于变性和坏死,同时给予转甲基化强效抑制剂S-腺苷-L-高半胱氨酸可抑制其作用。在胞苷二磷酸胆碱、磷脂酰胆碱和L-甲硫氨酸中未观察到保护作用。因此,在缺血后脑中提高脑内SAMe水平并以SAMe作为甲基供体激活转甲基化对于预防延迟性神经元死亡是必要的。