丁基苯酞对原代培养神经元线粒体功能的保护作用

The protective effects of butylphthalide on mitochondria against hypoxia/hypoglycaemia in cultured neurons

目的：探讨丁基苯酞（butylphthalide,NBP）对原代培养神经元在低糖低氧损伤下的保护作用及线粒体作用机制。方法：采用Hoechst 33342和PI共染的方法,观察NBP对低糖低氧损伤造成神经细胞坏死和凋亡的影响,并用荧光探针标记以及分光光度法检测NBP对神经细胞线粒体膜电位、线粒体膜流动性及线粒体呼吸链复合酶IV活性的影响。结果：NBP（10-6-10-4mol/L）能显著减少低糖低氧引起的神经细胞坏死和凋亡;机制研究表明它能明显改善由损伤引起的神经细胞线粒体膜电位、线粒体膜流动性及线粒体呼吸链复合酶IV活性的降低。结论：NBP对低糖低氧损伤导致的神经细胞坏死和凋亡具有良好的保护作用,而线粒体保护可能是其作用机制之一。

Objective： To investigate the protective effects of butylphthalide （NBP） on neuronal necrosis and apoptosls caused by hypoxia/hypoglycaemia, and its mitochondrial mechanisms. Methods： Dual stain with Hoechest 33342 and Propidium Iodide （PI） was used to detect the necrosis and apoptosis. Rhodamine - 123 （rhod - 123 ） and DPH were used as fluorescent indicators to measure the mitochondria membrane potential （MMP） and the mitochondria membrane fluidity （MFu）. The activity of complex IV of respiratory chain was detected by spectrophotometry. Results： NBP could remarkably reduce the neuronal necrosis and apoptosis caused by hypoxia./hypoglycemia. It could increase the MMP, MFu and the activity of complex IV, which were dropped during the hypoxia/hypoglycemia injury. Conclusions ： NBP could protect cultured neurons against hypoxia/hypoglycemia injury, and the mitochondria protection is involved in its mechanism.