Department of Anesthesiology, University Hospital of the RWTH Aachen, Pauwelsstraße 30, 52074 Aachen, Germany.
BMC Neurol. 2012 Apr 11;12:20. doi: 10.1186/1471-2377-12-20.
The α2-adrenoreceptor agonist dexmedetomidine is known to provide neuroprotection under ischemic conditions. In this study we investigated whether dexmedetomidine has a protective effect in an in vitro model for traumatic brain injury.
Organotypic hippocampal slice cultures were subjected to a focal mechanical trauma and then exposed to varying concentrations of dexmedetomidine. After 72 h cell injury was assessed using propidium iodide. In addition, the effects of delayed dexmedetomidine application, of hypothermia and canonical signalling pathway inhibitors were examined.
Dexmedetomidine showed a protective effect on traumatically injured hippocampal cells with a maximum effect at a dosage of 1 μM. This effect was partially reversed by the simultaneous administration of the ERK inhibitor PD98059.
In this TBI model dexmedetomidine had a significant neuroprotective effect. Our results indicate that activation of ERK might be involved in mediating this effect.
α2-肾上腺素受体激动剂右美托咪定在缺血情况下已知具有神经保护作用。在这项研究中，我们研究了右美托咪定是否对创伤性脑损伤的体外模型具有保护作用。
器官型海马切片培养物受到局灶性机械创伤，然后暴露于不同浓度的右美托咪定。72 小时后，使用碘化丙啶评估细胞损伤。此外，还检查了延迟给予右美托咪定、低温和经典信号通路抑制剂的效果。
右美托咪定对创伤性海马细胞具有保护作用，在 1 μM 剂量下作用最大。同时给予 ERK 抑制剂 PD98059 可部分逆转这种作用。
在这种 TBI 模型中，右美托咪定具有显著的神经保护作用。我们的结果表明，ERK 的激活可能参与介导这种作用。
