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个人信息Personal Information
教授
博士生导师
硕士生导师
性别:男
毕业院校:东北师范大学
学位:博士
所在单位:生物工程学院
电子邮箱:bioeng@dlut.edu.cn
Systemic administration of catalpol prevents D-galactose induced mitochondrial dysfunction in mice
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论文类型:期刊论文
发表时间:2010-04-12
发表刊物:NEUROSCIENCE LETTERS
收录刊物:SCIE、Scopus
卷号:473
期号:3
页面范围:224-228
ISSN号:0304-3940
关键字:Catalpol; Aging; Mitochondria; Respiratory complex; Mitochondrial membrane potential; Reactive oxygen species
摘要:The aim of this work was to evaluate the mechanisms involved in the effects of catalpol on mitochondrial function through the measurements of nitric oxide synthase (NOS) activity, reactive oxygen species (ROS) production, respiratory complex activities and mitochondrial membrane potential (MMP) in the brain cortex and hippocampus mitochondria of senescent mice induced by D-galactose. Except control group, mice were subcutaneously injected with D-galactose (150 mg/kg body weight) for 6 weeks. Meanwhile, drug group mice were treated with catalpol (2.5,5, 10 mg/kg body weight) and piracetam (300 mg/kg body weight) for the last 2 weeks. The results indicated that respiratory complex activities decreased while NOS activities increased in D-galactose treated mice brain. The production of ROS increased remarkably and MMP collapsed in the brain of senescent mice induced by ID-galactose. Administration of catalpol for 2 weeks significantly decreased ROS production and NOS activities, in accordance with its increase on complex activities and MMP level. Our results suggest that in vivo effects of catalpol on mitochondrial function can occur through different mechanisms, involving inhibiting NOS activity and ROS production, increasing respiratory complex activities and MMP level. (C) 2010 Elsevier Ireland Ltd. All rights reserved.