Alzheimer’s disease (AD) is the most common neurodegenerative disorder. The neuropathological hallmarks of AD include deposit of beta amyloid (Aβ) fibrils in senile plaques and a prominent role is exerted by inflammatory process. In the present study we analyzed in in vitro and in ex vivo model of AD the neuroprotective effects of the association of palmitoylethanolamide (PEA) with the antioxidant flavonoids luteolin (Lut), a compound obtained by a co-ultramicronization process (in a ratio 10:1 respectively). For in vitro model of AD we used a human neuroblastoma cell line SH-SY5Y, that was differentiated with Retinoic Acid (100 nM) and pre-treated with PEA-Lut (at three concentration 0.1-1-10 μM) for 2h. The damage was induced by Aβ1-42 stimulation (1µM). 24 hrs after damage we performed cell death assay (MTT) and western blot analysis for IκBα and NF-κB. Moreover, we carried out an ex vivo model of AD; to this purpose organotypic hippocampal slice cultures were prepared from P6 mice. Brains were transversely cut to obtain 400μm sections and placed onto semiporous inserts. On day 21 of culturing, organotypic hippocampal slides were pre-treated with PEA-Lut (0.1-1-10 μM) for 2h, and the damage was induced by Aβ1-42 (1μg/ml). 24hrs after damage, sections were gently removed from inserts and processed for MTT assay, NO assay and western blot analysis. Our data indicate that PEA-Lut association is able to blunt Aβ-induced astrocyte activation and to exert a marked protective effect on glial cells, providing an effective strategy for AD.

Neuroprotection by association of palmitoylethanolamide with luteolin in experimental Alzheimer’s disease models: the control of neuroinflammation

Cordaro Marika;Irene Paterniti;Campolo Michela;Rosalba Siracusa;Emanuela Esposito;Salvatore Cuzzocrea
2014-01-01

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disorder. The neuropathological hallmarks of AD include deposit of beta amyloid (Aβ) fibrils in senile plaques and a prominent role is exerted by inflammatory process. In the present study we analyzed in in vitro and in ex vivo model of AD the neuroprotective effects of the association of palmitoylethanolamide (PEA) with the antioxidant flavonoids luteolin (Lut), a compound obtained by a co-ultramicronization process (in a ratio 10:1 respectively). For in vitro model of AD we used a human neuroblastoma cell line SH-SY5Y, that was differentiated with Retinoic Acid (100 nM) and pre-treated with PEA-Lut (at three concentration 0.1-1-10 μM) for 2h. The damage was induced by Aβ1-42 stimulation (1µM). 24 hrs after damage we performed cell death assay (MTT) and western blot analysis for IκBα and NF-κB. Moreover, we carried out an ex vivo model of AD; to this purpose organotypic hippocampal slice cultures were prepared from P6 mice. Brains were transversely cut to obtain 400μm sections and placed onto semiporous inserts. On day 21 of culturing, organotypic hippocampal slides were pre-treated with PEA-Lut (0.1-1-10 μM) for 2h, and the damage was induced by Aβ1-42 (1μg/ml). 24hrs after damage, sections were gently removed from inserts and processed for MTT assay, NO assay and western blot analysis. Our data indicate that PEA-Lut association is able to blunt Aβ-induced astrocyte activation and to exert a marked protective effect on glial cells, providing an effective strategy for AD.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3145114
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