右美托咪定对大鼠神经元缺氧无糖损伤保护作用的实验研究

Protection and mechanism of dexmedetomidine preconditioning against neuronal injury related to oxygen-glucose deprivation

目的研究a2肾上腺素受体激动剂右美托咪定(dexmedetomidine,DEX)对原代培养的大鼠皮层神经元缺氧无糖损伤(OGD)的保护作用并探讨其机制。方法建立原代培养的大鼠皮层神经元缺氧无糖损伤(OGD)模型,通过采用MTT、LDH等方法观察右美托咪定对于神经元缺氧无糖损伤的保护作用,Western blot检测p38MAPK蛋白表达的变化。结果右美托咪定对于缺氧无糖(OGD)损伤处理的神经元具有明显保护效果。右美托咪定预处理显著降低OGD损伤神经元中的磷酸化p38MAPK蛋白表达,p38MAPK抑制剂SB203580能模拟DEX的神经保护作用,使细胞存活率升高。结论右美托咪定预处理对于大鼠原代皮层神经元OGD损伤具有明显的保护效果。其机制可能与通过降低磷酸化p38MAPK表达有关。

Objective To study the protection and mechanism ofdexmedetomidine preconditioning against neuronal injury related to oxygen - glucose deprivation（OGD）. Methods Cortical neurons from the embryonic day 16-18 rats were cultured. With mimicking a cerebral ischemia in vitro, OGD was performed in the pretreated cells. Neuron injury was assessed by MTT. Protein expression of p-p38 was examined by Western blot. Results Dexrnedetomidine preconditioning protected the dose-dependent cortical neurons from OGD injury. Conclusions Dexmedetomidine preconditioning protects the cortical neuron from OGD injury; inhibition of p38MAPK pathway maybe one of the mechanisms responsible for this effect.