线粒体损伤在阿维菌素致体外培养神经细胞凋亡中的作用

Avermectin-induced mitochondria damage and apoptosis in cultured pigeon neurons

通过体外培养王鸽脑神经细胞,并按终浓度0、2.5、5和10μg/L阿维菌素(AVM)染毒,培养24 h时,经透射电镜观察神经细胞超微结构,DNA断裂评价细胞凋亡,MTT法测定线粒体活性,酶标仪检测Caspase-3、Caspase-9活性,流式细胞术测定线粒体跨膜电位(Δψm),探讨线粒体损伤在AVM致体外培养神经细胞凋亡中的作用。结果显示,AVM可明显抑制神经细胞线粒体的活性,引起Δψm下降,Caspase-3和Caspase-9活性升高,神经细胞发生凋亡,存在明显的剂量效应关系。证实,线粒体损伤是AVM致体外培养神经细胞凋亡的机理之一。

Cultured primary King pigeon brain neurons were exposed to avermectin （AVM） at concen-trations of 0,2.5,5 and 10μg/L for 24 hours. Ultrastructures of the neurons were evaluated by transmission electron microscope. DNA fragmentations were used as an indication of cell apoptosis. Mitochondria activity was determined by the MTT method. Activities of Caspases-3 and -9 were determined by Immuno-analyser. Flow cytometry was used to determine the changes of mitochondria transmembrane potential （△ψm）. Results showed that AVM inhibited neuronal mitochondria activity, decreased the △ψm, and in- creased the activities of Caspases-3 and -9. They indicated that AVM could induce the apoptosis of the cultured brain neurons through mitochondria injury.