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
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摘要: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.Abstract:Objective To study the effects of dipfluzine(Dip)against lead-induced injury in primary cultured hippocampal neurons and explore its mechanism.Methods The primary cultured hippocampal neurons were treated with PbAc2 to establish injury model.The cell viability, lactate dehy drogenase(LDH)leakage rate and intr acellularCa2+i in cultures were measured to study the protective effect of Dip.Results Dip(1.0 μmol/Land 10 μmol/L)could lighten the damage of cultured hippocampal neurons induced by lead.Dip(1.0Lmol/Land 10 μmol/L)incr eased the cell viability and decreased the LDHleakage rate of cultured hippocampal neurons(P < 0.01).Dip(0.1 μmol/L, 1.0 μmol/Land 10 μmol/L)could decrease intracellularCa2+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 intr acellular calcium overload in neurons.
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