梓醇对鱼藤酮所致小鼠脑线粒体损伤的保护作用  

Protective Effect of Catalpol Against Mice Brain Mitochondrial Injuries Induced by Rotenone

作　　者：石桂芳[1,2] 王贺双[3,2] 毛玉荣[2] 刘晓燕[2] 姜波[2] 

机构地区：[1]大连美罗中药厂有限公司产品研发部,辽宁大连116036 [2]大连理工大学生命科学与技术学院,辽宁大连116024 [3]大连市中心医院中心实验室,辽宁大连116100

出　　处：《现代生物医学进展》2012年第29期5661-5664,共4页Progress in Modern Biomedicine

基　　金：科技部国际科技合作重点项目计划(No.2005DFA40790)

摘　　要：目的:研究梓醇对鱼藤酮所致小鼠脑线粒体损伤的保护作用。方法:小鼠随机分为对照组、模型组和治疗组。模型组腹腔注射鱼藤酮21d;治疗组先注射鱼藤酮21 d,后用梓醇治疗10 d。测定小鼠中脑、纹状体和皮层中线粒体复合酶Ⅰ、谷胱甘肽(GSH)、乳酸脱氢酶(LDH)活性、膜电位、活性氧(ROS)的含量。结果:梓醇能够提高小鼠复合酶Ⅰ活性,增加GSH的含量,减少膜电位的丢失和活性氧的生成,抑制LDH的释放。结论:梓醇对鱼藤酮损伤小鼠脑线粒体具有保护作用。ABSTRACT Objective： To study the effect of catalpol on the mitochondrial function of mice brain mitochondrial on rotenone-induced damage in mice. Methods： Mice were randomly divided into three group, control group, model group and therapy group. Model group was injected intraperitoneally （i.p.） with rotenone （1.5 mg/kg） for 21 days, therapy group was injected with rotenone for 21 days, then given catalpol （10 mg/kg） for 10 days. The activities of complex I and lactic dehydrogenase （LDH）, mitochondrial membrane potential, content of reduced glutathione （GSH） and reactive oxygen species （ROS） in midbrain, striatum and cortex mitochondria of mice were assayed. Results： Catalpol could increase the activities of complex I, increase GSH contents, decrease the loss of mitochondrial membrane potential and restrain the release of LDH. Conclusion： Catalpol has protective effect on mice brain mitochondrial injury induced by rotenone. Key words： Catalpol; Rotenone; Mice; Mitochondria

关 键 词：梓醇 鱼藤酮 小鼠 线粒体 

分 类 号：Q95-3[生物学—动物学] R742.5[医药卫生—神经病学与精神病学]