Icariin ameliorates neuropathological changes, TGF-β1 accumulation and behavioral deficits in a mouse model of cerebral amyloidosis

PLoS One. 2014 Aug 7;9(8):e104616. doi: 10.1371/journal.pone.0104616. eCollection 2014.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Protein Precursor / biosynthesis*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Behavior, Animal / drug effects*
  • Disease Models, Animal
  • Female
  • Flavonoids / pharmacology*
  • Humans
  • Mice
  • Mice, Transgenic
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism*

Substances

  • APP protein, human
  • Amyloid beta-Protein Precursor
  • Flavonoids
  • Tgfb1 protein, mouse
  • Transforming Growth Factor beta1
  • icariin

Grants and funding

Chaoyun Li is supported and financed by the Chinese government scholarship from the China Scholarship Council (CSC). The authors also acknowledge support by Deutsche Forschungsgemeinschaft (German Research Foundation) and Open Access Publishing Fund of Tuebingen University, for the open access publishing. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.