Rao A M, Başkaya M K, Maley M E, Kindy M S, Dempsey R J
Department of Neurological Surgery, Clinical Science Center, University of Wisconsin, Madison 53792-3232, USA.
Brain Res Mol Brain Res. 1997 Feb;44(1):134-8. doi: 10.1016/s0169-328x(96)00245-8.
We have studied the beneficial effects of S-adenosyl-L-methionine (SAM) tosylate on blood-brain barrier (BBB) breakdown and neuronal survival after transient cerebral ischemia in gerbils. BBB breakdown experiments were performed in pentobarbital anesthetized gerbils subjected to 10 min of bilateral carotid artery occlusion and 6 h of reperfusion. For BBB breakdown measurements, SAM (120 mg/kg, i.p.) was administered to gerbils just after occlusion and thereafter every hour up to 5 h. Fluorometric measurements quantified the blood-brain permeability tracer, Evans blue (EB). SAM treatment significantly reduced the BBB breakdown as indicated by reduced levels of EB fluorescence. Neuronal count experiments were conducted in gerbils subjected to transient ischemia and 7 days of reperfusion. For neuronal count experiments SAM (15-120 mg/kg) was administered at 6 and 12 h after reperfusion, and twice each day thereafter for 7 days. SAM dose dependently protected the hippocampal CA1 neurons assessed by histopathological methods. SAM has a beneficial effect on the outcome of ischemic injury by reducing the BBB breakdown and neuronal death.
我们研究了甲苯磺酸S-腺苷-L-甲硫氨酸（SAM）对沙土鼠短暂性脑缺血后血脑屏障（BBB）破坏和神经元存活的有益作用。在戊巴比妥麻醉的沙土鼠中进行BBB破坏实验，使其双侧颈动脉闭塞10分钟并再灌注6小时。为了测量BBB破坏情况，在闭塞后立即给沙土鼠腹腔注射SAM（120mg/kg），此后每小时注射一次，持续5小时。荧光测量法定量血脑通透性示踪剂伊文思蓝（EB）。SAM治疗显著减少了BBB破坏，表现为EB荧光水平降低。在经历短暂性缺血和7天再灌注的沙土鼠中进行神经元计数实验。对于神经元计数实验，在再灌注后6小时和12小时给予SAM（15-120mg/kg），此后每天两次，持续7天。通过组织病理学方法评估，SAM剂量依赖性地保护海马CA1神经元。SAM通过减少BBB破坏和神经元死亡，对缺血性损伤的结果具有有益作用。
