王静云

个人信息Personal Information

教授

博士生导师

硕士生导师

性别:女

毕业院校:大连理工大学

学位:博士

所在单位:生物工程学院

学科:生物化工. 生物工程与技术. 药物工程

办公地点:生物楼512

联系方式:wangjingyun67@dlut.edu.cn

电子邮箱:wangjingyun67@dlut.edu.cn

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D-galactose administration induces memory loss and energy metabolism disturbance in mice: Protective effects of catalpol

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论文类型:期刊论文

发表时间:2008-08-01

发表刊物:FOOD AND CHEMICAL TOXICOLOGY

收录刊物:SCIE、PubMed、Scopus

卷号:46

期号:8

页面范围:2888-2894

ISSN号:0278-6915

关键字:rehmannia; catalpol; aging; neuroprotection; learning and memory; energy metabolism

摘要:The neuroprotective effects of catalpol, an iridoid glycoside isolated from the fresh rehmannia roots, on the behavior and brain energy metabolism in senescent mice induced by D-galactose were assessed. Except control group, mice were subcutaneously injected with D-galactose (150 mg/kg body weight) for 6 weeks. From the fifth week, 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. Behavioral changes including open field test and passive avoidance were examined after drug administration. To determine the brain damage, pathological alterations were measured by hematoxylin and eosin (HE) staining. The activities of lactate dehydrogenase (LDH), glutathione S-transferase (GSH-ST), glutamine synthetase (GS), creatine kinase (CK) in brain cortex and hippocampus were determined using different biochemical methods. Consistent with the cognition deficits, the activities of GSH-ST, GS and CK decreased while the activity of LDH increased in aging mice brain. Administration of catalpol for 2-weeks not only ameliorated cognition deficit, but also reversed the biochemical markers mentioned above and reduced the histological lesions in mouse brain. These results suggest that catalpol has protective effects oil memory damage and energy metabolism failure in aging model mice and is worth testing for further preclinical study aimed for senescence or neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). (c) 2008 Elsevier Ltd. All rights reserved.