摘要
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.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2007年第5期73-76,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
2007年北京市自然基金预探索项目(No:07E0044)
2004年度留学回国人员科技活动择优资助项目
2006年北京市属市管高等学校人才强教计划资助项目
关键词
丁基苯酞
凋亡
线粒体膜电位
细胞膜流动性
呼吸链复合酶
butylphthalide
apoptosis
mitochondria membrane potential
mitochondria membrane fluidity
complex IV of respiratory chain