Oxidative stress has been associated to neuronal cell loss in neurodegenerative diseases.Neurons are post-mitotic cells that are very sensitive to oxidative stress--especially considering theirlimited capacity to be replaced. Therefore, reduction of oxidative stress, and inhibiting apoptosis,will potentially prevent neurodegeneration. In this study, we investigated the neuroprotective eectof Ginkgo biloba extract (EGb 761) against H2O2 induced apoptosis in SK-N-BE neuroblastoma cells.We analysed the molecular signalling pathway involved in the apoptotic cell death. H2O2 inducedan increased acetylation of p53 lysine 382, a reduction in mitochondrial membrane potential,an increased BAX/Bcl-2 ratio and consequently increased Poly (ADP-ribose) polymerase (PARP)cleavage. All these eects were blocked by EGb 761 treatment. Thus, EGb 761, acting as intracellularantioxidant, protects neuroblastoma cells against activation of p53 mediated pathway and intrinsicmitochondrial apoptosis. Our results suggest that EGb 761, protecting against oxidative-stressinduced apoptotic cell death, could potentially be used as nutraceutical for the prevention andtreatment of neurodegenerative diseases.
Ginkgo biloba Prevents Oxidative Stress-Induced Apoptosis Blocking p53 Activation in Neuroblastoma Cells
Francesco Di Meo;Sabrina Margarucci;Stefania Filosa
;Stefania Crispi
2020
Abstract
Oxidative stress has been associated to neuronal cell loss in neurodegenerative diseases.Neurons are post-mitotic cells that are very sensitive to oxidative stress--especially considering theirlimited capacity to be replaced. Therefore, reduction of oxidative stress, and inhibiting apoptosis,will potentially prevent neurodegeneration. In this study, we investigated the neuroprotective eectof Ginkgo biloba extract (EGb 761) against H2O2 induced apoptosis in SK-N-BE neuroblastoma cells.We analysed the molecular signalling pathway involved in the apoptotic cell death. H2O2 inducedan increased acetylation of p53 lysine 382, a reduction in mitochondrial membrane potential,an increased BAX/Bcl-2 ratio and consequently increased Poly (ADP-ribose) polymerase (PARP)cleavage. All these eects were blocked by EGb 761 treatment. Thus, EGb 761, acting as intracellularantioxidant, protects neuroblastoma cells against activation of p53 mediated pathway and intrinsicmitochondrial apoptosis. Our results suggest that EGb 761, protecting against oxidative-stressinduced apoptotic cell death, could potentially be used as nutraceutical for the prevention andtreatment of neurodegenerative diseases.File | Dimensione | Formato | |
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