Mechírová Eva, Domoráková Iveta, Danková Marianna, Danielisová Viera, Burda Jozef
Department of Histology and Embryology, Faculty of Medicine, PJ Safárik University in Kosice, 04180 Kosice, Slovak Republic.
Cell Mol Neurobiol. 2009 Sep;29(6-7):991-8. doi: 10.1007/s10571-009-9386-2. Epub 2009 Mar 17.
Short term sublethal ischemia or ischemic preconditioning gives protection to the neurons against subsequent lethal ischemic attack. This so-called ischemic tolerance can also be provided by certain drugs. We examined the effect of noradrenalin and EGb 761 on the spinal cord neurons injured by 30 min occlusion of abdominal aorta in rabbits. The animals survived 48 and 72 h. Degenerated neurons were visualized by Fluoro Jade B method, viable neurons were demonstrated immunohistochemically with NeuN and ubiquitin antibodies. The rabbits with noradrenalin administration 48 h before 30 min of ischemia and 48/72 h of reperfusion, showed significant increase of degenerated Fluoro Jade B labeled neurons. Animals of both groups were paraplegic. Rabbits pretreated 7 days with EGb 761 prior to 30 min of ischemia and with 48/72 h of reperfusion revealed significant decrease of Fluoro Jade B-positive neurons when compared with the groups with 30 min of ischemia followed by 48/72 h of reperfusion. In the NeuN sections, the number of viable neurons was moderately decreased. These animals showed no paraplegia. Ubiquitin aggregates occurred in the cytoplasm of degenerated neurons in the sections of rabbits preconditioned with noradrenalin 48 h prior to 30 min of ischemia and followed by 48 h of reperfusion while after 72 h of reperfusion, shrunk light shadows without ubiquitin reaction were visible. Our results indicate that EGb 761 could be involved in protection of spinal cord neurons against ischemic injury while effect of noradrenalin is not unambiguous.
短期亚致死性缺血或缺血预处理可保护神经元免受随后的致死性缺血攻击。这种所谓的缺血耐受性也可由某些药物提供。我们研究了去甲肾上腺素和银杏叶提取物EGb 761对兔腹主动脉闭塞30分钟所致脊髓神经元损伤的影响。动物存活48小时和72小时。用Fluoro Jade B法观察变性神经元,用NeuN和泛素抗体免疫组化显示存活神经元。在缺血30分钟及再灌注48小时/72小时前48小时给予去甲肾上腺素的兔子,Fluoro Jade B标记的变性神经元显著增加。两组动物均出现截瘫。在缺血30分钟及再灌注48小时/72小时前7天用EGb 761预处理的兔子,与缺血30分钟后再灌注48小时/72小时的组相比,Fluoro Jade B阳性神经元显著减少。在NeuN切片中,存活神经元数量中度减少。这些动物未出现截瘫。在缺血30分钟前48小时用去甲肾上腺素预处理并再灌注48小时的兔子切片中,变性神经元的细胞质中出现泛素聚集物,而在再灌注72小时后,可见无泛素反应的收缩淡影。我们的结果表明,EGb 761可能参与保护脊髓神经元免受缺血损伤,而去甲肾上腺素的作用并不明确。