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Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke

Neural Regeneration Research 2019年第6期14卷 948-953页

作者： Jiamei Shen radhika rastogi Xiaokun Geng Yuchuan Ding China-America Institute of Neuroscience Beijing Luhe HospitalCapital Medical University Department of Neurosurgery Wayne State University School of Medicine Department of Neurology Beijing Luhe HospitalCapital Medical University

Nicotinamide adenine dinucleotide phosphate oxidase(NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however,excess reactive oxygen species generated by NOX promotes apoptotic cell death. In ischemic stroke, in particular, it has been shown that both NOX activation and derangements in glucose metabolism result in increased apoptosis. Moreover, recent studies have established that glucose, as a NOX substrate, plays a vital role in the pathogenesis of reperfusion injury. Thus, NOX inhibition has the potential to mitigate the deleterious impact of hyperglycemia on stroke. In this paper, we provide an overview of this research,coupled with a discussion of its implications for the development of NOX inhibition as a strategy for the treatment of ischemic stroke. Both inhibition using apocynin, as well as the prospect of developing more specific inhibitors based on what is now understood of the biology of NOX assembly and activation, will be highlighted in the course of our discussion.

关键词： nicotinamide adenine dinucleotide phosphate oxidase stroke nicotinamide adenine dinucleotide phosphate oxidase inhibitors reactive oxygen species ischemia/reperfusion neuroprotection hyperglycolysis NADPH NOX

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