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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 5763743, 11 pages
http://dx.doi.org/10.1155/2016/5763743
Research Article

Immediate Remote Ischemic Postconditioning Reduces Brain Nitrotyrosine Formation in a Piglet Asphyxia Model

1Preclinical Neonatal Neuroprotection Group, UCL EGA Institute for Women’s Health, London WC1E 6BT, UK
2Department of Pharmacology, UCL School of Pharmacy, London WC1N 1AX, UK
3Perinatal Brain Group, UCL EGA Institute for Women’s Health, London WC1E 6HX, UK

Received 22 January 2016; Revised 21 March 2016; Accepted 27 March 2016

Academic Editor: Serafina Perrone

Copyright © 2016 Eridan Rocha-Ferreira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Remote ischemic postconditioning (RIPostC) is a promising therapeutic intervention that could be administered as an alternative to cooling in cases of perinatal hypoxia-ischemia (HI). In the current study we hypothesized that RIPostC in the piglet model of birth asphyxia confers protection by reducing nitrosative stress and subsequent nitrotyrosine formation, as well as having an effect on glial immunoreactivity. Postnatal day 1 (P1) piglets underwent HI brain injury and were randomised to HI (control) or HI + RIPostC. Immunohistochemistry assessment 48 hours after HI revealed a significant decrease in brain nitrotyrosine deposits in the RIPostC-treated group (). This was accompanied by a significant increase in eNOS expression () and decrease in iNOS (), with no alteration in nNOS activity. Interestingly, RIPostC treatment was associated with a significant increase in GFAP () and IBA1 (), markers of astroglial and microglial activity, respectively. The current study demonstrates a beneficial effect of RIPostC therapy in the preclinical piglet model of neonatal asphyxia, which appears to be mediated by modulation of nitrosative stress, despite glial activation.