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Using quantitative immunohistochemistry, modifications of HIF-1alpha expression in neocortex of rats exposed to various modes of mild hypobaric hypoxia (MHH) (1,3 and 6 episodes) differed in their neuroprotective efficacy have been studied. It has been shown that three-trial MHH being the most effective neuroprotective mode when used as a preconditioning produces most considerable changes in HIF-1 by substantial up-regulation of its regulatory alpha-subunit expression in the rat neocortex. Present findings support the hypothesis on important roles of HIF-1 in the mechanisms of brain hypoxic tolerance induced by the hypoxic preconditioning with three-trial MHH.

Transcription factor NF-kappaB plays a pivotal role in mechanisms of brain neuron survival and degeneration under injurious stimuli, first of all different types of hypoxia. In the present work, using quantitative immunohystochemistry, we provide analysis of expression of different subunits of NF-kappaB (p65 and c-Rel) in the rat neocortex in response to severe injurious hypobaric hypoxia (HH) or after a single or multiple sessions of mild protective HH. Severe hypoxia (SH), resulting in loss of brain neurons, has no effect on the level of expression of p65 but suppresses expression of c-Rel. Multiple (but not single one) trials of preconditioning using mild HH which reduce neuronal damage promote p65 expression and prevent suppression of c-Rel level after SH. Triple session of mild HH itself when applied as a preconditioning stimulus upregulate expression of both subunits, while single administration or sixfold trials has no effect on the level of immunoreactivity of both subunits. The revealed peculiarities of the expression of p65 and c-Rcl implies that these subunits of NF-kappaB appear to contribute to the mechanisms of brain tolerance to SH.