Abstract
Icariin, a major constituent of flavonoids from the Chinese medicinal herb Epimedium brevicornum, exhibits multiple biological properties, including anti-inflammatory, neuroregulatory and neuroprotective activities. Therefore, Icariin might be applied in treatment of neurodegenerative disorders, including Alzheimer's disease (AD), which is neuropathologically characterized by β-amyloid aggregation, hyperphosphorylated tau and neuroinflammation. Potential therapeutic effects of Icariin were investigated in an animal model of cerebral amyloidosis for AD, transgenic APP/PS1 mouse. Icariin was suspended in carboxymethylcellulose and given orally to APP/PS1 mice. Therapeutic effects were monitored by behavioral tests, namely nesting assay, before and during the experimental treatment. Following an oral treatment of 10 days, Icariin significantly attenuated Aβ deposition, microglial activation and TGF-β1 immunoreactivity at amyloid plaques in cortex and hippocampus of transgenic mice 5 months of age, and restored impaired nesting ability. Our results suggest that Icariin might be considered a promising therapeutic option for human AD.
Highlights
Icariin is a natural flavonoid extracted from the Chinese tonic herb Epimedium and is considered the major pharmacologically active compound
Icariin shows antidepressant-like activity [6]; protects against aluminium-induced learning and memory deficits due to its antioxidant activities; decreases Ab1-40 content in the hippocampus of aluminium-intoxicated rodents [7]; and its metabolite Icaritin has neuroprotective effects on b amyloid-induced neurotoxicity to neuronal cells [8]
As a baseline of this assay, an impaired nesting ability of these transgenic mice was confirmed in our previous study, compared to age- and gender matched naıve mice [21]
Summary
Icariin is a natural flavonoid extracted from the Chinese tonic herb Epimedium and is considered the major pharmacologically active compound. Previous studies reported that Icariin ameliorated brain dysfunction induced by LPS [2], inhibited corticosterone-induced apoptosis in neurons [3], attenuated the ischemia/reperfusion damage to neurons [4], stimulated neurite growth [5] and thereby showed antineuroinflammatory and neuroprotective activities. Icariin shows antidepressant-like activity [6]; protects against aluminium-induced learning and memory deficits due to its antioxidant activities; decreases Ab1-40 content in the hippocampus of aluminium-intoxicated rodents [7]; and its metabolite Icaritin has neuroprotective effects on b amyloid-induced neurotoxicity to neuronal cells [8]. It is proposed that Ab peptides are toxic and causative in AD, contributing to memory loss, behavioral impairment and neurodegenerative pathology [9]. As a potent immunomodulator and with a central role in the response to neuroinflammation, TGF-b1 is considered to be involved in pathological progression of AD
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