Matsui Y, Kubo Y, Iwata N
Biological Research Laboratories, Sankyo Co. Ltd., Tokyo, Japan.
Eur J Pharmacol. 1987 Dec 1;144(2):211-6. doi: 10.1016/0014-2999(87)90521-8.
The effect of S-adenosyl-L-methionine (SAM) on neuronal degeneration induced by transient forebrain ischemia was studied in rats. Bilateral occlusion of the common carotid arteries for 30 min in a 4-vessel occlusion model caused degeneration of CA1 neurons of the hippocampus. When SAM-HCl or SAM sulphate tosylate (SAM-ST, 100 mg/kg as the free form of SAM, i.p.) was administered just after recirculation and every hour for 5 h after recirculation, the degeneration and loss of pyramidal cells were prevented. However, adenosine, a metabolite of SAM, and glycerol, which has the same osmotic pressure as the solution of SAM-ST, did not show any effects on the neuronal damage. The results showed that SAM has a beneficial effect on neuronal damage induced by ischemia.
研究了S-腺苷-L-甲硫氨酸(SAM)对大鼠短暂性前脑缺血诱导的神经元变性的影响。在四血管闭塞模型中,双侧颈总动脉闭塞30分钟会导致海马CA1神经元变性。当在再灌注后立即给予盐酸SAM或甲苯磺酸SAM(SAM-ST,以SAM的游离形式计100mg/kg,腹腔注射)并在再灌注后每小时给药一次,持续5小时时,锥体细胞的变性和丢失得到了预防。然而,SAM的代谢产物腺苷以及与SAM-ST溶液具有相同渗透压的甘油对神经元损伤没有任何影响。结果表明,SAM对缺血诱导的神经元损伤具有有益作用。