ИСТИНА

Postconditioning (PostC) is an exposure of the damaged organism to extreme factors of the mild intensity to mobilize endogenous protective mechanisms. Method of PostC, which consists of three sequential episodes of mild hypobaric hypoxia, has recently been developed and validated in our laboratory. This model of hypoxic PostC was shown to improve the rats` rehabilitation after injurious severe hypobaric hypoxia (SH) by preventing neuronal loss, normalizing the lipid peroxidation process, the activity of the endocrine system and animal behaviour. In particular, it was demonstrated that hypoxic PostС up-regulates hypoxia-inducible factor-1 alpha subunits (HIF1a) level in the CA1 field of the hippocampus. Here, we have tested the hypothesis that hypoxic PostC induces neuroprotection through HIF1-dependent stimulation of pentose phosphate pathway activity. We have proved that SH suppresses the glucose-6-phosphate dehydrogenase activity in rat hippocampus, which leads to attenuation of reduced NADPH, total and reduced glutathione levels. This data correlate with decreased total antioxidant activity of cytosolic and mitochondrial subcellular fractions of rat hippocampus in this group. Meanwhile, hypoxic PostC normalizes the activity of glucose-6-phosphate dehydrogenase, stabilizes the NADP reduction process and causes a significant grow in total and reduced glutathione quantity and the rise of total antioxidant activity in the rat hippocampus. The excess reactive oxygen species generation is considered to provoke hypoxia-mediated neuronal death. Therefore, stabilization of processivity of antioxidant systems can play a key role in preventing the consequences of reoxygenation.