Danielisova Viera, Gottlieb Miroslav, Bonova Petra, Nemethova Miroslava, Burda Jozef
Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia.
Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia.
Neurochem Int. 2014 Jun;72:22-9. doi: 10.1016/j.neuint.2014.04.005. Epub 2014 Apr 18.
The goal of this study is to investigate the effects of bradykinin (BR) postconditioning on cerebral ischemic injury. Transient focal cerebral ischemia was induced in rats by 60min of middle cerebral artery occlusion (MCAO), followed by 3days of reperfusion. BR as a postconditioner at a dose of 150μg/kg was applied intraperitoneally 3, 6, 24 and 48h after MCAO. BR postconditioning significantly reduced total infarct volumes if applied 3h after MCAO by 95%, 6h after MCAO by 80% and 24h after MCAO by 70% in versus vehicle group. Neurological functions were amarked improvement in the BR groups compared to the ischemia group. The number of degenerated neurons in the hippocampal CA1 region was also significantly lower in BR-treated ischemic groups compared to vehicle group. BR postconditioning prevented the release of MnSOD from the mitochondria and reduced the activity of the total SOD and CAT if it is administrated short time after stroke. Our data proves the ischemic tolerance in the brain induced by BR postconditioning resulted as effective agent against as strong an attack as 60min MCAO even when used many hours after ischemia.
本研究的目的是探讨缓激肽（BR）后处理对脑缺血损伤的影响。通过大脑中动脉闭塞（MCAO）60分钟诱导大鼠短暂局灶性脑缺血，随后再灌注3天。在MCAO后3、6、24和48小时腹腔注射剂量为150μg/kg的BR作为后处理剂。与载体组相比，MCAO后3小时应用BR后处理可使总梗死体积显著减少95%，MCAO后6小时减少80%，MCAO后24小时减少70%。与缺血组相比，BR组的神经功能有明显改善。与载体组相比，BR处理的缺血组海马CA1区变性神经元的数量也显著减少。如果在中风后短时间给药，BR后处理可防止线粒体中MnSOD的释放，并降低总SOD和CAT的活性。我们的数据证明，BR后处理诱导的脑缺血耐受性是一种有效的药物，即使在缺血数小时后使用，也能抵抗60分钟MCAO这样强烈的攻击。
