MacMillan V, Walton-Roche K, Davis J
Division of Neurology, University of Toronto, Ontario, Canada.
Can J Neurol Sci. 1993 Feb;20(1):37-40. doi: 10.1017/s0317167100047375.
Occlusion of the carotid arteries for 5 minutes in the Mongolian gerbil results in selective necrosis of CA1 pyramidal neurons. In the present experiments we studied whether intraventricular infusion of acidic fibroblast growth factor (aFGF) could attenuate this damage. Intraventricular infusions of bovine serum albumin (BSA-10 ng/h) or aFGF (1, 10 or 100 ng/h) were started 2 days prior to 5 minutes of bilateral carotid occlusion and continued for 5 days post-ischemia. The brains were perfused and fixed at 5 days post-ischemia and histological assessment of CA1 damage was made. Animals receiving intraventricular infusions of 10 or 100 ng/h aFGF showed a significant reduction of CA1 neuronal damage in comparison to no treatment ischemic controls (no treatment-8 +/- 1; aFGF 10 ng/h-147 +/- 28; aFGF 100 ng/h-168 +/- 35 cells/mm CA1; P < 0.05 for both aFGF groups). The results indicate that aFGF infusion can attenuate the severity of ischemic neuronal necrosis in the gerbil hippocampus.
在蒙古沙鼠中,颈动脉闭塞5分钟会导致CA1锥体神经元发生选择性坏死。在本实验中,我们研究了脑室内注入酸性成纤维细胞生长因子(aFGF)是否能减轻这种损伤。在双侧颈动脉闭塞5分钟前2天开始脑室内注入牛血清白蛋白(BSA - 10 ng/h)或aFGF(1、10或100 ng/h),并在缺血后持续5天。在缺血后5天对大脑进行灌注和固定,并对CA1损伤进行组织学评估。与未治疗的缺血对照组相比,接受脑室内注入10或100 ng/h aFGF的动物CA1神经元损伤显著减少(未治疗组 - 8 ± 1;aFGF 10 ng/h组 - 147 ± 28;aFGF 100 ng/h组 - 168 ± 35个细胞/mm CA1;两个aFGF组P均< 0.05)。结果表明,注入aFGF可减轻沙鼠海马区缺血性神经元坏死的严重程度。