尼莫地平对脑挫裂伤后神经细胞内游离钙浓度的影响

Effects of nimodipine on intracellular free Ca^(2+) concentration and apoptosis in rat neural cells following cerebral contusions

目的研究尼莫地平对脑挫裂伤后神经细胞胞浆内游离钙离子浓度变化的影响。方法将Wistar大鼠随机分为对照组、创伤组、治疗组;创伤组按照Feeney自由落体脑损伤模型方式制作大鼠左顶叶脑挫裂伤模型,治疗组在外伤后开始静脉滴注尼莫地平。分别对脑挫裂伤后0.5、1、3、6、12、24、48 h各时相点细胞内游离钙离子浓度和细胞凋亡率进行检测。对不同时相的创伤组、治疗组和对照组进行比较分析。结果脑挫裂伤后大脑皮层神经细胞内游离钙离子浓度迅速升高,0.5 h时为正常值的4倍,24 h时达到高峰,48 h时降低明显,但仍然维持在比较高的水平。应用尼莫地平治疗后,钙离子浓度显著降低,6 h时降至接近正常水平。脑挫裂伤后神经细胞凋亡率和胞内游离钙离子浓度存在相关性。结论脑挫裂伤后神经细胞胞浆内钙离子浓度升高,导致钙超载并引起细胞凋亡。早期应用尼莫地平能抑制钙超载,抑制细胞凋亡,对神经细胞具有极强的保护作用。

Objective To study the effects of nimodipine on intracellular free Ca^2＋ concentration in rat neurocytes following cerebral contusions. Methods Wistar rats were randomly divided into three groups： the control group, the traanma group and the treatment group. The cerebral contusion models were established based on the Feeney method and nimodipine was immediately administered after cerebral contusions. The related parameters at different times after cerebral contusion were detected. Intracellular free Ca^2＋ concentration and apoptosis rate were determined by flow cytometry. Results After cerebral contusion, intracellular free Ca^2＋ concentration was increased and reached a peak at 24 h and then gradually decreased, but it still maintained a high level at 48 h, while nimodipine made the intracellular free Ca^2＋ concentration remarkably decrease and the Ca^2＋ level was decreased to the normal level at 6h （94.85 ± 15.63 nmol/L）. Conclusion Intracellular free Ca^2＋concentration is related to apoptosis rate. Nimodipine can decrease the Ca^2＋ levels and has some protective role against cerebral contusion.