| 丁基苯酞对原代培养神经元线粒体功能的保护作用 |
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| 引用本文： | 熊杰,徐平湘,孙丽娜,成亮,冯亦璞,王晓良.丁基苯酞对原代培养神经元线粒体功能的保护作用[J].中药药理与临床,2007,23(5):73-76. |
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| 作者姓名： | 熊杰 徐平湘 孙丽娜 成亮 冯亦璞 王晓良 |
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| 作者单位： | 1. 首都医科大学化学生物学与药学院药理系,北京,100069
2. 中国医学科学院,中国协和医科大学药物研究所,北京,100050 |
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| 基金项目： | 北京市自然科学基金预探索项目;留学回国人员科技活动择优资助项目;北京市属市管高校人才强教计划 |
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| 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。
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| 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 |
The protective effects of butylphthalide on mitochondria against hypoxia/hypoglycaemia in cultured neurons |
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| Xiung Jie,Xu Pingxiang,Sun lina,Cheng Liang,Feng Yipu,Wang Xiaoliang.The protective effects of butylphthalide on mitochondria against hypoxia/hypoglycaemia in cultured neurons[J].Pharmacology and Clinics of Chinese Materia Medica,2007,23(5):73-76. |
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| Authors: | Xiung Jie Xu Pingxiang Sun lina Cheng Liang Feng Yipu Wang Xiaoliang |
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| Institution: | 1 Department of Pharmacology, School of Chemical Biology and Pharmaeal Science, Capital Medical University, Beijing 100069 ; 2 Institute of Materia Mediea, Chinese Aeedimy of Medical Seienees . Peking Union Medical Colloge, Beijing 100050 |
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| Abstract: | Objective: To investigate the protective effects of butylphthalide(NBP) on neuronal necrosis and apoptosis 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. |
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| Keywords: | butylphthalide apoptosis mitochondria membrane potential mitochondria membrane fluidity complex IV of respiratory chain |
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