NP7 protects from cell death induced by oxidative stress in neuronal and glial midbrain cultures from parkin null mice |
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Authors: | MA Mena MJ Casarejos JA Rodríguez-Navarro I Rodal JG de Yebenes |
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Institution: | a Departmento de Neurobiología-Investigación, CIBERned, Hospital Ramón y Cajal, Carretera de Colmenar, km 9, Madrid 28034, Spain b Department of Neurobiology, CIBERned, Hospital Ramon y Cajal, 28034 Madrid, Spain c Noscira, Tres Cantos, Madrid, Spain |
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Abstract: | Parkin mutations produce Parkinson’s disease (PD) in humans and nigrostriatal dopamine lesions related to increased free radicals in mice. We examined the effects of NP7, a synthetic, marine derived, free radical scavenger which enters the brain, on H2O2 toxicity in cultured neurons and glia from wild-type (WT) and parkin null mice (PK-KO).NP7, 5-10 μM, prevented the H2O2 induced apoptosis and necrosis of midbrain neuronal and glial cultures from WT and PK-KO mice. NP7 suppressed microglial activation and the H2O2 induced drop-out of dopamine neurons. Furthermore, NP7 prevented the increased phosphorylation of ERK and AKT induced by H2O2. NP7 may be a promising neuroprotector against oxidative stress in PD. |
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Keywords: | Parkinson&rsquo s disease Parkin knockout mice Dopamine neurons Glia Oxidative stress Apoptosis p-ERK and p-AKT signaling pathways Aged glia |
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