作者: Qing Lu , Valerie A. Harris , Sanjv Kumar , Heidi M. Mansour , Stephen M. Black
DOI: 10.1016/J.REDOX.2015.06.016
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摘要: Autophagy is activated when the neonatal brain exposed to hypoxia ischemia (HI), but mechanisms underlying its activation and role in neuronal cell death associated with HI unclear. We have previously shown that reactive oxygen species (ROS) derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase play an important HI-mediated death. Thus, aim of this study was determine if ROS involved autophagy injury a protective or deleterious pathway. Initial electron microscopy data demonstrated autophagosome formation elevated P7 hippocampal slice cultures oxygen-glucose deprivation (OGD). This corresponded increased levels LC3II mRNA protein. The inhibitor, 3-methyladenine (3-MA) effectively reduced OGD. Neuronal significantly attenuated. Finally, we found pharmacologic inhibition NADPH using apocynin gp91ds-tat decreased rat respectively. our results suggest contributes oxidative stress dependent.