双苯氟嗪对铅致海马神经元损伤的保护作用

Protective effect of dipfluzine on lead-induced injury in cultured primary hippocampal neurons

目的观察双苯氟嗪(Dipfluzine,Dip)对铅致原代培养海马神经元损伤的保护作用,并探讨其作用机制。方法以原代培养的海马神经元作为研究对象,用醋酸铅造海马神经元损伤模型,通过测定细胞存活率,乳酸脱氢酶(LDH)泄漏率和胞内游离钙浓度(〔Ca2+i〕),观察Dip对铅致原代培养海马神经元损伤的保护作用。结果Dip 1.0和10μmol/L可显著提高铅损伤海马神经元存活率,降低LDH泄漏率,对铅诱导的海马神经元〔Ca2+〕i升高有明显的抑制作用(P<0.01);Dip 0.1μmol/L亦可抑制铅诱导的海马神经元〔Ca2+〕i升高(P<0.05)。结论Dip对铅致原代培养海马神经元损伤具有保护作用,其机制可能与其抑制铅诱导的胞内钙超载有关。

Objective To study the effects of dipfluzine （Dip） against lead - induced injury in primary cultured hippoeampal neurons and explore its mechanism. Methods The primary cultured hippocampal neurons were treated with PbAe2 to establish injury model. The cell viability, lactate dehydrogenase （LDH） leakage rate and intracellular [Ca^2＋ ]i in cultures were measured to study the protective effect of Dip. Results Dip （1.0 μmol/L and 10 μmol/L） could lighten the damage of cultured hippocampal neurons induced by lead. Dip （1.0 μmol/L and 10 μmol/L） increased the cell viability and decreased the LDH leakage rate of cultured hippoeampal neurons （ P 〈 0.01 ）. Dip （0.1 μmol/L, 1.0 μmol/L and 10 μmol/L） could decrease intracellular [Ca^2＋ ]i（P 〈 0.01 or P 〈 0.05）. Conclusion Dip holds protective effect against lead - induced injury in cultured hippocampal neurons, which is possibly due to inhibiting the intraeellular calcium overload in neurons.