Neurotoxicity Research

, Volume 6, Issue 2, pp 119–130

Neuroprotective effect ofH. perforatum extracts on β-amyloid-induced neurotoxicity

Authors

  • Bruno A. Silva
    • Institute of Biochemistry and Center for Neuroscience and Cell Biology of Coimbra, Faculty of MedicineUniversity of Coimbra
    • Laboratory of Plant Molecular Biochemistry and Physiology, Department of BiologyUniversity of Minho
  • Alberto C. P. Dias
    • Laboratory of Plant Molecular Biochemistry and Physiology, Department of BiologyUniversity of Minho
  • Federico Ferreres
    • Research Group on Quality, Safety and Bioactivity of Plant FoodsCEBAS (CSIC)
    • Institute of Biochemistry and Center for Neuroscience and Cell Biology of Coimbra, Faculty of MedicineUniversity of Coimbra
  • Catarina R. Oliveira
    • Institute of Biochemistry and Center for Neuroscience and Cell Biology of Coimbra, Faculty of MedicineUniversity of Coimbra
Article

DOI: 10.1007/BF03033214

Cite this article as:
Silva, B.A., Dias, A.C.P., Ferreres, F. et al. neurotox res (2004) 6: 119. doi:10.1007/BF03033214

Abstract

In the present study we assessed the neuroprotective role of aHypericum perforatum ethanolic extract and obtained fractions in amyloid-β peptide (Aβ)(25–35)-induced cell death in rat cultured hippocampal neurons. Lipid peroxidation was used as a marker of oxidative stress by following the formation of TBARS in rat cortical synaptosomes, after incubation with ascorbate/Fe2+, alone or in the presence of EC97 effective concentrations ofH. perforatum fractions. Induced lipid peroxidation was significantly inhibited by fractions containing flavonol glycosides, flavonol and biflavone aglycones, and by a fraction containing several phenols, mainly chlorogenic acid-type phenolics (21%,77%and 98%, respectively). Lipid peroxidation evaluated after incubation with 25 μM Aβ(25–35), was significantly inhibited byH. perforatum extract.

Cell viability was assessed by use of the Syto-13/PI assay. The total ethanolic extract (TE) and fractions containing flavonol glycosides, flavonol and biflavone aglycones, reduced Aβ(25–35)-induced cell death (65%,58%and 59%,respectively). These results were further supported by morphological analysis of cells stained with cresyl violet. Peptide β-amyloid(25–35) induced a decrease in cell volume, chromatin condensation and nuclear fragmentation, alterations not evident in the presence of the TE and fractions containing hypericins (hypericin concentration = 11.02 μM), or fractions containing flavonoids (quercetin concentration = 21.13 μM). Dendritic lesion,an evidence of neurodegeneration, was observed by neuronal staining with cobalt following insult with Aβ(25–35), but prevented after exposure to the peptide plus the fractions referred above.

The results of the present paper suggest thatH. perforatum extracts may be endowed with neuroprotective compounds able to prevent Aβ(25–35)-induced toxicity.

Keywords

Alzheimer’s diseaseHypericum perforatumAmyloid β(25–35)NeuroprotectionHippocampal neurons

Copyright information

© Springer 2004