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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。
In order to explore the protective effect of nimodipine on cerebral nerve cells, neurons of 24 female SD rats were cultured in vitro and divided into normal control group, hypoxic-ischemic group and nimodipine-treated group. Eight rats in each group were used to observe the change of total calcium (Ca2 +) and free calcium (Ca2 + i) in cytoplasm of three groups of animals. Results: The levels of TCa2 + and Ca2 + i in the hypoxic-ischemic group were significantly higher than those in the normal group (TCa2 + 3, 6 .70 ± 1.15 μg / ml and 1.08 ± 0.14F331.2 / F382.4, respectively) .10 ± 1.15 μg / ml cell and Ca2 + i0.83 ± 0.13F331.2 / F382.4) (P <0.05). The levels of TCa2 + and Ca2 + i in the nimodipine-treated group were 3.5 3 μg / ml cells ± 1.74 and 0.89 ± 0.05 F331.2 / 382.4, respectively, which were significantly lower than those in hypoxic-ischemic group (P <0.05), but no significant difference compared with normal group P> 0 .0 5). This suggests that nimodipine can block the cerebral neuronal hypoxic-ischemic injury of calcium overload, can effectively protect brain cells.