论文部分内容阅读
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 investigate the protective effect of dexmedetomidine (DEX), an a2-adrenoceptor agonist, on primary cultured rat cortical neurons against oxygen-glucose-free injury (OGD) and its possible mechanism. Methods Primary cultured rat cortical neurons were established with hypoxia and sugarless injury (OGD) model. MTT and LDH were used to observe the protective effects of dexmedetomidine on hypoxic-glucose-deficient neurons. Western blot was used to detect the expression of p38MAPK Changes in protein expression. Results Dexmedetomidine had a significant protective effect on neurons treated with hypoxic-glucose-free (OGD) injury. Dexmedetomidine preconditioning significantly reduced phosphorylated p38MAPK protein expression in OGD-injured neurons, and p38MAPK inhibitor SB203580 mimics the neuroprotective effect of DEX, resulting in an increase in cell survival. Conclusion Dexmedetomidine pretreatment has obvious protective effect on OGD injury in rat primary cortical neurons. The mechanism may be related to the decrease of phosphorylated p38MAPK expression.