In the present study we assessed the neuroprotective role of a
Hypericum 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/Fe
2+, alone or in the presence of EC
97 effective concentrations of
H. 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 by
H. 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 disease - Hypericum perforatum - Amyloid β(25–35)
- Neuroprotection - Hippocampal neurons