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| Amyloid beta-peptide (Aβ) has been proposed as a model of Alzheimer’s disease (AD) as it has neurotoxicity and induces neuronal loss and cognitive decline similar to the features of AD. Catalpol, an iridoid glycoside richly in the roots of Rehmannia glutinosa, was found to have protective effects on neurodegenerative diseases in our previous experiment. The aim of this study was to assess the neuroprotective effects of catalpol against Aβ induced neurotoxicity and learning impairment in rats. The rats were divided into control group, AD-model group, sham-operated group, therapy group and prevention group. Except control and sham-operated group, Aβ1-42 was injected into the rat hippocampus to establish AD model after or before subcutaneous injection of catalpol (10 mg/kg, 5 days). The rats of therapy and prevention group showed significantly improved learning and memory ability in Morris water maze test compared with those of AD-model group. Further study showed that catalpol increased the activities of acetylcholinesterase (AChE), Na+-K+-ATPase and Ca2+ -ATPase in the hippocampus of Aβ treated rats. Simultaneously, catalpol remarkably increased ChAT positive neurons by immunohistochemical staining and reduced the histological lesions by hematoxylin and eosin (HE) staining in the hippocampus of therapy and prevention group rats. All the data indicated that catalpol might prevent and treat Aβ1-42 –induced damage in rat model and be worth studying for further preclinical study aimed for AD. |
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| Keywords:catalpol; Aβ1-42; hippocampus; cognitive; cholinergic |
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