Institute of Neurobiology, Slovak Academy of Sciences, Soltesovej 4/6, Kosice, SK-040 01, Slovakia.
Neurochem Int. 2013 Jan;62(1):8-14. doi: 10.1016/j.neuint.2012.10.015. Epub 2012 Nov 7.
The period from stroke initiation to the cessation of penumbra damage spread represents a therapeutic window when expansion can be alleviated. In the present work, we studied some biochemical parameters helpful for the estimation of infarct progression and thus for the application of interventions. We designed four groups: the control group and three groups of animals after middle cerebral artery occlusion with reperfusion periods of 2h, 1day or 3days. In the ischaemic core and penumbra, fluorimetric and spectrophotometric methods for investigating total MnSOD and MAO-A/B activity as well as level of the glutamate were used. Protein synthesis was assessed by in vitro measurements of (14)C-leucine incorporation. Noticeable differences between core and penumbra biochemical parameters were shown. In the core, protein synthesis was transiently inhibited two hours and three days after ischaemia (36%). Glutamate and total SOD activity peaked on the first day, but on the third day after MCAO, rapidly decreased by about 44% and 33.6%, respectively. In the penumbra, ischaemia led to higher protein synthesis (78%), elevations in glutamate and rapid activation of MnSOD (by about 884%) one day after insult. On the third day, protein synthesis and MnSOD were still significantly elevated (36% and 388%, respectively), while glutamate levels returned to baseline. In addition, the impact of ischaemia on MAO-A/B activity in the penumbra was confirmed. In conclusion, biochemical parameter screening could be helpful to assess cell damage progress and the possibility of rescue. These regions reflect different biochemical patterns that seem to be clearly established on the first day after transient MCAO. Moreover, the first day of post-ischaemic reperfusion in the present model of stroke seems to be the breakpoint, i.e. the time at which expanding cell death from the infarct core to the penumbra can be at least partially eliminated.
从中风发作到半影损伤停止的时间代表了一个治疗窗口，在此期间可以缓解扩张。在本工作中，我们研究了一些有助于估计梗死进展的生化参数，从而有助于应用干预措施。我们设计了四个组：对照组和三个大脑中动脉闭塞后再灌注 2 小时、1 天或 3 天的动物组。在缺血核心和半影区，使用荧光和分光光度法研究总 MnSOD 和 MAO-A/B 活性以及谷氨酸水平。通过体外测量（14）C-亮氨酸掺入来评估蛋白质合成。显示核心和半影区生化参数之间存在明显差异。在核心区，缺血后 2 小时和 3 天蛋白质合成短暂抑制（36%）。谷氨酸和总 SOD 活性在第一天达到峰值，但在 MCAO 后第三天，分别迅速下降约 44%和 33.6%。在半影区，缺血导致更高的蛋白质合成（78%），谷氨酸升高，并在损伤后一天迅速激活 MnSOD（约 884%）。第三天，蛋白质合成和 MnSOD 仍然显著升高（分别为 36%和 388%），而谷氨酸水平恢复到基线。此外，还证实了缺血对半影区 MAO-A/B 活性的影响。总之，生化参数筛选有助于评估细胞损伤进展和挽救的可能性。这些区域反映了不同的生化模式，这些模式似乎在短暂 MCAO 后第一天就已经明确建立。此外，在本中风模型中，缺血后第一天似乎是一个转折点，即从梗死核心向半影区扩展的细胞死亡至少可以部分消除的时间。
