Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na+/K+ ATPases

• DOI: 10.1038/s41419-018-0656-0
• Publication Date: 2018-05-25T08:57:25Z
• Authors: Haixia Wen; Liu Liu; Lixuan Zhan; Donghai Liang; Luxi Li; Dandan Liu; Weiwen Sun; En Xu
• Keywords: Neuroglobin

Abstract Hypoxic postconditioning (HPC) is an innovative neuroprotective strategy with cytoprotective effects on the hippocampal neurons against transient global cerebral ischemia (tGCI) in adult rats. However, its molecular mechanisms have not yet been adequately elucidated. Neuroglobin (Ngb) endogenous neuroprotectant hypoxia-inducible property, and role experimental stroke has increasingly attractive. Hence, purpose of this study to explore involvement Ngb HPC-mediated neuroprotection further investigate underlying mechanism. We found that HPC increased expression CA1 subregion after tGCI. Also, inhibition antisense oligodeoxynucleotide (AS-ODNs) eliminated effect mediated by HPC, whereas overexpression ameliorated neuronal damage tGCI, indicating conferred via upregulation Ngb. showed membranous level Na + /K ATPases β1 subunit (Atp1b1) Furthermore, we demonstrated maintained Atp1b1 through Ngb–Atp1b1 interaction reduced glutathionylation suppression reactive oxygen species (ROS), ultimately preserving activity NKA. Taken together, these data indicate involved tGCI maintenance NKA CA1.