木犀草素对大鼠皮层神经元氧化损伤的保护作用  

Luteolin protected cultured cortical neurons from oxidative stress-induced damage

作　　者：陈瑶玥[1] 暨荀鹤[1] 郭礼和[1] 

机构地区：[1]中科院上海生命科学研究院生物化学与细胞生物学研究所,上海200031

出　　处：《中国药理学通报》2008年第3期382-386,共5页Chinese Pharmacological Bulletin

基　　金：上海市科委重大科技攻关资助项目(No05DZ19339)

摘　　要：目的研究木犀草素对于皮层神经元氧化损伤的保护作用及其机制。方法用200μmol·L-1H2O2处理皮层神经元造成神经元的氧化损伤,用LDH活性检测细胞死亡,MTT测定线粒体活性,荧光分光检测神经元线粒体膜电位,细胞内ROS的积累以及过氧化氢酶和谷胱甘肽的含量变化。结果20μmol·L-1的木犀草素能有效的保护H2O2导致的神经元死亡,有效维护线粒体膜电位和线粒体活性,减少细胞内ROS的累积,并能通过提高细胞内谷胱甘肽的含量有效对抗氧化损伤,同时对于H2O2造成的过氧化氢酶活力和谷胱甘肽含量的急剧下降也有很好的保护作用。结论木犀草素是一种比较有效的对抗神经元氧化损伤的保护剂,它很可能通过维持线粒体的活性而达到神经保护作用,并通过提高细胞内谷胱甘肽的水平,增强神经元抗氧化损伤的能力。Aim To examine the effect of Luteolin on H2O2 induced damage in cultured cortical neurons. Methods Cortical neurons were exposed to 200 μmol · L^-1 H2O2 for 12 hours and the cell toxicity of H2O2 was evaluated by LDH release. MTT assay was used to elucidate the mitochondrial activity. Mitochondrial transmembrane potential, intracellular reactive oxygen species, catalase activity and glutathione were measured by spectrofluorophotometer. Results 200 μmol·L^-1 H2O2 induced great damage to mitochondria and caused death in primary cultured cortical neurons. 20 μmol · L^-1 Luteolin effectively protected neurons from oxidative damage, maintained the mitochondrial activity as well as transmenmbrane potential, decreased the ROS accumulation and kept the activity of the antioxidant system. What is more, increasing the GSH level by Luteolin pretreatment might improve the antioxidant ability of neurons. Conclusions Luteolin protects cortical neurons from H2O2 toxicity by inhibiting the damage to the mitochondria and improving the antioxidant ability of neurons.

关 键 词：木犀草素 皮层神经元 H2O2 氧化损伤 

分 类 号：R-332[医药卫生] R284.1