The aim of the study was to investigated on Delayed Luminescence emitted by an in vitro model concerning the effects of amyloid-β (Aβ). Aβ is a neurotoxic protein overexpressed in Alzheimer's Disease (AD), which is also related to mitochondrial dysfunction. The experiments have been carried out on Olfactory Ensheathing Cells (OECs) cultures. The cells have been exposed to Aβ(1-42) native full-length peptide or to Aβ(25-35), a toxic fragment of Aβ, or Aβ(35-25), a no toxic Aβ fragment both in the absence and in the presence of Astaxanthin, a well-known antioxidant. DL intensity and kinetics changes also as a function of the treatments were measured. In particular, an increase in DL emission, when compared with the untreated cells used as control, was observed when the cells were exposed to Aβ(25-35) fragment. This emission appears quenched in presence of Astaxanthin.
Delayed Luminescence by an in vitro model for the study of mechanism involved in neurodegenerative diseases
R. GRASSO;R. PELLITTERI;F. MUSUMECI;V. RAPICAVOLI;G. SPOSITO;A. TRIGLIA;A. SCORDINO;A. CAMPISI
2020-01-01
Abstract
The aim of the study was to investigated on Delayed Luminescence emitted by an in vitro model concerning the effects of amyloid-β (Aβ). Aβ is a neurotoxic protein overexpressed in Alzheimer's Disease (AD), which is also related to mitochondrial dysfunction. The experiments have been carried out on Olfactory Ensheathing Cells (OECs) cultures. The cells have been exposed to Aβ(1-42) native full-length peptide or to Aβ(25-35), a toxic fragment of Aβ, or Aβ(35-25), a no toxic Aβ fragment both in the absence and in the presence of Astaxanthin, a well-known antioxidant. DL intensity and kinetics changes also as a function of the treatments were measured. In particular, an increase in DL emission, when compared with the untreated cells used as control, was observed when the cells were exposed to Aβ(25-35) fragment. This emission appears quenched in presence of Astaxanthin.File | Dimensione | Formato | |
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