NP7 protects from cell death induced by oxidative stress in neuronal and glial midbrain cultures from parkin null mice

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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. © 2008 Federation of European Biochemical Societies.

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Mena, M. A., Casarejos, M. J., Solano, R., Rodríguez-Navarro, J. A., Gómez, A., Rodal, I., … de Yebenes, J. G. (2009). NP7 protects from cell death induced by oxidative stress in neuronal and glial midbrain cultures from parkin null mice. FEBS Letters, 583(1), 168–174. https://doi.org/10.1016/j.febslet.2008.11.051

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