d-galactose administration induces memory loss and energy metabolism disturbance in mice: protective effects of catalpol.
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 on 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).
Zhang
Xiu-Li
XL
School of Environmental and Biological Science and Technology, Dalian University of Technology, Dalian 116024, China.
An
Li-Jia
LJ
Bao
Yong-Ming
YM
Wang
Jing-Yun
JY
Jiang
Bo
B
D000375:Aging / Q000502:physiology / Q000523:psychology; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D003071:Cognition / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D005690:Galactose / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D005960:Glucosides / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D007202:Indicators and Reagents; D057888:Iridoid Glucosides; D039823:Iridoids / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008569:Memory Disorders / Q000139:chemically induced* / Q000523:psychology; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D018517:Plant Roots / Q000737:chemistry; D032267:Rehmannia / Q000737:chemistry
D005960:Glucosides; D007202:Indicators and Reagents; D057888:Iridoid Glucosides; D039823:Iridoids; C078040:catalpol; D007770:L-Lactate Dehydrogenase; D005982:Glutathione Transferase; D003402:Creatine Kinase; D005978:Glutathione; D005690:Galactose