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The effect of hypoxic postconditioning after severe hypobaric hypoxia on the expression of Cu, Zn-SOD in hippocampus and neocortex of rats

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SpringerPlus20154 (Suppl 1) :P45

  • Published:


  • Postconditioning
  • hypoxia
  • Cu, Zn-superoxide dismutase

Oxidative stress is a key mechanism of cellular damage during and after severe hypoxia. Accordingly, up-regulation of expression and activity of endogenous antioxidants is an important mechanism of cellular adaptation to hypoxia. Do endogenous antioxidants take part in postconditioning-induced neuroprotective mechanisms similarly to their participation in preconditioning-induced ones? In the present work the effect of postconditioning by 3-trial mild hypobaric hypoxia (360 Torr, 2 h, once a day) after 1 session of severe acute hypobaric hypoxia (180 Torr, 3 h) on the expression of Cu, Zn-superoxide dismutase (Cu, Zn-SOD) was studied by immunocytochemical analysis in areas CA1, CA2, CA3, CA4 and DG of hippocampus and in frontoparietal neocortex (NC) of male Wistar rats. Two time points were examined: 3 h after the last session of postconditioning that was 3 days after severe hypoxia and 24 h after the last session of postconditioning that was 4 days after severe hypoxia. It has been shown that postconditioning significantly increases the total number of Cu, Zn-SOD-immunoreactive cells (Nt) at least in two areas of hippocampus studied (CA2 and DG) compared to non-postconditioned rats at 3 days but not at 4 days after severe hypoxia. In contrast, in NC of postconditioned rats, Nt tends to increase compared to non-postconditioned animals at 4 days but not at 3 days after severe hypoxia. The effect of postconditioning on the number of intensely expressing Cu, Zn-SOD neurons differs in various areas and at various time points. The modification of Cu, Zn-SOD expression in some areas of hippocampus and NC, induced by 3-trial hypoxic postconditioning, correlates with the prevention of massive delayed apoptotic neuronal death and amelioration of functional disorders caused by severe hypoxia. Thus, Cu, Zn-SOD and other endogenous antioxidants may play, apparently, an important role in the treatment of severe hypoxia/ischemia stroke by postconditioning in brain neurons.

Authors’ Affiliations

School of Medicine, University of Tampere, Finland
I.P. Pavlov Institute of Physiology of RAS, Russian Federation, Russia


© Stroev et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.