S-adenosyl-L-methionine protects the hippocampal CA1 neurons from the ischemic neuronal death in rat.
S-adenosyl-L-methionine protects the hippocampal CA1 neurons from the ischemic neuronal death in rat.
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DOI：
10.1016/0006-291x(88)90547-5
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发表时间：
1988-01
影响因子：
3.1
通讯作者：
H. Sato;H. Hariyama;K. Moriguchi
中科院分区：
文献类型：
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作者：
H. Sato;H. Hariyama;K. Moriguchi
我们研究了S-腺苷-L-甲硫氨酸（SAMe）对短暂性前脑缺血大鼠迟发性神经元死亡的预防作用。作为结果，SAMe剂量依赖性地保护海马CA 1神经元免于变性和坏死，其效果被同时施用S-腺苷-L-同型半胱氨酸（一种有效的转甲基化抑制剂）抑制。CDP-胆碱、磷脂酰胆碱和L-蛋氨酸均无保护作用。因此，提高脑内SAMe水平，以SAMe为甲基供体激活脑内的甲基转移，对预防迟发性神经元死亡是必要的。
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.