摘要
为探讨尼莫地平对脑神经细胞的保护作用 ,将 2 4只雌性 SD大鼠的大脑皮层神经细胞经试管内培养后 ,分为正常对照组、缺氧缺血组和尼莫地平处理组 ,每组各 8只 ,观察并比较 3组动物神经细胞胞浆总钙(TCa2 + )和游离钙 (Ca2 + i)的变化。结果 :缺氧缺血组神经细胞 TCa2 +和 Ca2 + i分别为 6 .70± 1.15 μg/ m l cell和 1.0 8± 0 .14F331.2 / F382 .4,均明显高于正常组 (TCa2 + 3 .10± 1.15 μg/ ml cell和 Ca2 + i0 .83± 0 .13F331.2 / F382 .4)(P<0 .0 5 ) ;尼莫地平处理组 TCa2 +和 Ca2 + i分别为 3.5 3μg/ ml cell± 1.74和 0 .89± 0 .0 5 F331.2 / 382 .4,均明显低于缺氧缺血组 (P<0 .0 5 ) ,但与正常组比较则无显著性差异 (P>0 .0 5 )。由此提示 ,尼莫地平可阻滞脑神经细胞缺氧缺血性损伤时的钙超载 ,能有效地保护脑神经细胞。
This study aimed to investigate the changes of total calcium (TCa 2+ ) and free calcium ion(Ca 2+ i) concentrations in cortical neurons in rats and hence to elucidate the protective effect of nimodipine on hypoxic ischemic brain damage (HIBD). Twenty four female SD rats were divided into three groups: normal control group ( n =8); 20mmol/L CNK group (i.e.HIBD group, n =8); 20mmol/L CNK+100mmol/L nimodipine treatment(antagonist group, n =8). TCa 2+ and Ca 2+ i in neuron cytoplasm were measured in the cortical neuron cultures. The findings showed that the neuronal TCa 2+ and Ca 2+ i concentrations (TCa 2+ 6.70±1.15μg/ml cell and Ca 2+ i 1 08±0.14 F331.2/F382.4) in HIBD group were significantly higher than those(TCa 2+ 3.10±1.15μg/ml cell and Ca 2+ i 0.83±0.13 F331.2/F382.4) in normal control group ( P <0.05). The neuronal TCa 2+ and Ca 2+ i concentrations (TCa 2+ 3.53±1.74μg/ml cell and Ca 2+ i 0.89±0.05 F331.2/F382.4) in antagonist group were lower than those in HIBD group ( P <0.05). The results suggest that intracellular calcium accumulation is associated with hypoxic ischemic brain damage, and that calcium antagonist, nimodipine, is effective in protecting brain cells from further damage through its influence on rat cortical neuronal calcium accumulation.
出处
《华西医科大学学报》
CSCD
2000年第4期506-507,共2页
Journal of West China University of Medical Sciences
基金
国家教委博士学科点专项基金
关键词
尼莫地平
缺氧缺血性脑病
脑神经细胞
钙
Cortical neuron culture Nimodipine Hypoxic ischemic brain damage Calcium
