目的：探讨钙及钙调蛋白依赖性激酶（calmodulin dependent kinase,CaMK）在神经元缺氧损伤中的作用及机制。方法：体外培养大鼠胚脑皮质神经元，随机分为单纯缺氧组及钙阻滞剂干预组，其中钙阻滞剂干预组采用尼莫地平（nimodipine）、MK-801分别阻断L-VSCC受体、NMDA受体的传导，采用MTT法测定各组神经元缺氧前后细胞活性，用Fluo-4AM荧光探针测定各组细胞内钙离子浓度的变化，Western blot检测CaMKⅡ及CaMKⅣ的表达。结果：尼莫地平及MK-801组细胞活性较单纯缺氧的对照组高；尼莫地平可迅速降低缺氧神经元的细胞内钙， MK-801可长时间降低缺氧神经元的细胞内钙。尼莫地平可抑制CaMKⅡ的表达，MK-801对CaMKⅡ的表达无明显影响,但可抑制CaMK Ⅳ的表达。结论：尼莫地平和MK-801可分别通过抑制CaMKⅡ和CaMKⅣ表达实现对缺氧神经元的保护作用。［中国当代儿科杂志，2007，9（4）：324-326］

OBJECTIVE: To study the effects of calcium and calmodulin dependent kinase against hypoxic neuronal injury and its possible mechanisms. MethodsEmbryonic cortical neurons of 17-day pregnant embryo Sprague-Dawley rats were cultured in vitro and the cultured neurons were randomly allocated into different groups that exposed to hypoxia or hypoxia +calcium channel antagonist. Nimodipine and MK-801 were used to block the L-voltage sensitive calcium channel and NMDA receptor respectively before hypoxia. The methyl thiazolyl tetrazolium(MTT) method was used to determine the cell viability. Fluo-4AM, an intracellular calcium indictor, was used to detect the changes of intracellular calcium after hypoxia. The expressions of CaMKⅡ and CaMKⅣ were detected by Western blot. ResultsThe cell viability of the nimodipine or MK-801-treated groups was significantly higher than that of the untreated hypoxia group. The intracellular calcium level of the nimodipine-treated group decreased rapidly after hypoxia. Compared to nimodipine treatment, MK-801 treatment could inhibit hypoxia-induced calcium influx for a longer time. Nimodipine treatment decreased the CaMKⅡexpression while MK-801 treatment decreased the CaMKⅣ expression. CONCLUSIONS: Nimodipine and MK-801 protect neurons from hypoxic injury possibly by the inhibition of CaMKⅡ and CaMKⅣ expressions respectively.［Chin J Contemp Pediatr, 2007, 9 (4):324-326］