异氟醚激活ERK和HIF-1α产生对神经元缺氧无糖损伤的保护作用

目的　探讨异氟醚预处理在对大鼠皮层神经元缺氧损伤中的保护作用及其可能机制。 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，采用MTT法观察异氟醚对神经元OGD损伤的保护作用,Western blot检测磷酸化ERK（pERK）和低氧诱导因子(HIF)-1α蛋白表达。 结果　异氟醚预处理显著增加OGD损伤神经元中HIF-1α的蛋白含量,ERK抑制剂PD98059可以部分阻断这种作用。 结论　异氟醚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。其机制可能与通过增加pERK表达,进而调节HIF-1α的表达有关。

Protection and mechanism of isoflurane preconditioning against oxygen-glucose deprivation neuronal injury

Objective　To study the protection and mechanism of isoflurane preconditioning against oxygen-glucose deprivation(OGD) neuronal injury.　Methods　Cortical neurons from rats at embryonic day 16 to 17 were cultured. With simuation of a cerebral ischemia in vitro, OGD was performed in the pretreated cells. Neuron injury was assessed by MTT. Protein expressionof pERK and HIF-1α was determined by Western blot. Results　Isoflurane preconditioning protected dose-dependently the cortical neuron from OGD injury. The hypoxia inducible factor (HIF-1α) in the OGD injured neurons was increased by isoflurane preconditioning, which was partially abolished by ERK inhibitor PD98059.　Conclusions　Isoflurane preconditioning protects the cortical neuron from OGD injury, possibly through activating HIF-1α mediated by pERK.