阿司匹林对化学性缺氧状态下新生大鼠脑神经细胞[Ca2+]i和NGB的影响

目的 探讨阿司匹林(ASA)对化学性缺氧大鼠脑神经细胞的保护作用及细胞外钙离子对ASA神经保护作用的影响。方法 分别在含钙和去钙培养液中加入连二亚硫酸钠（Na2S2O4）诱导化学性缺氧,用ASA预处理体外培养的大鼠脑细胞,激光共聚焦显微镜观察[Ca2+]i和脑红蛋白（NGB）的变化。结果 化学性缺氧使大鼠脑细胞[Ca2+]i和NGB表达增高（P＜0.05, n=5）。ASA预处理可明显缓解缺氧组和无钙缺氧组大鼠脑细胞[Ca2+]i和NGB的增高（P＜0.05, n=5）。结论 ASA可能通过减少大鼠脑细胞的钙超载,抑制缺氧诱导的NGB表达增高,发挥神经细胞保护作用。

Effects of aspirin on [Ca~(2+)] i and NGB in cultured neural cells of newborn rat under chemical-induced hypoxic exposure

Objective To investigate the protective effects of aspirin on hypoxic brain neural cells of rat and the effects of extracellular calcium on the neuroprotective effect of aspirin. Methods The hypoxic cell model was established by adding Na_2S_2O_4 to the calcium or calcium free medium. Cultured primary cortical neurons of rat were pretreated with ASA in vitro. The change of intracellular free calcium and neuroglobin (NGB) were observed and analyzed by laser scanning confocal microscope. Results The expression level of [Ca~(2+)] i and NGB increased significantly in the chemical hypoxia group ( P < 0. 05 ). ASA can attenuate the increase of [ Ca~(2+) ] i and NGB in the hypoxic group and calcium-free hypoxia group(P <0. 05). Conclusion Aspirin can inhibit calcium overload and the hypoxia-induced expression of NGB, so protect rat brain cells against hypoxia.