Related Experiment Video
Updated: Jun 27, 2026

Primary Culture of Mouse Dopaminergic Neurons
Published on: September 8, 2014
NP7 protects from cell death induced by oxidative stress in neuronal and glial midbrain cultures from parkin null
M A Mena1, M J Casarejos, R Solano
1Departmento de Neurobiología-Investigación, CIBERned, Hospital Ramón y Cajal, Madrid, Spain. maria.a.mena@hrc.es
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 H(2)O(2) toxicity in cultured neurons and glia from wild-type (WT) and parkin null mice (PK-KO). NP7, 5-10 microM, prevented the H(2)O(2) induced apoptosis and necrosis of midbrain neuronal and glial cultures from WT and PK-KO mice. NP7 suppressed microglial activation and the H(2)O(2) induced drop-out of dopamine neurons(.) Furthermore, NP7 prevented the increased phosphorylation of ERK and AKT induced by H(2)O(2). NP7 may be a promising neuroprotector against oxidative stress in PD.