Changes in the Expression of Antiapoptotic Protein Bcl-2 in the Rat Neocortex and Hippocampus in Different Hypobaric Hypoxia Regimes

Abstract

Studies during the 1980s demonstrated delayed neuron death in hippocampal fi eld CA1 several days after ischemia [7]. Subsequent studies also produced similar fi ndings in other parts of the brain with high sensitivity to hypoxia/ ischemia – the neocortex, striatum, and cerebellum. This type of neuron damage was shown to be linked with the mechanism of induction of apoptosis (programmed cell death), which involve genes and killer proteins [8]. A central position in the regulation of the mechanisms of apoptosis is occupied by proteins of the bcl-2 gene family – the proapoptotic Bax and Bcl-xs and the antiapoptotic Bcl-2 and Bcl-xL [6, 9, 10]. Induction of apoptosis after harmful exposure to ischemia/hypoxia in susceptible areas of the brain is associated with increases in the content of proapoptotic and decreases in the content of antiapoptotic proteins. Studies in the early 1990s identifi ed another phenomenon – “ischemic/hypoxic brain tolerance,” induced before the harmful effects of moderate, so-called preconditioning (PC) ischemia/hypoxia, which to a signifi cant extent prevents neuron death in susceptible areas of the brain [1]. PC with moderate hypobaric hypoxia (MHH) was showed to be able to eliminate the structural-functional damage to hippocampal and neocortical neurons, and also to be able to change the ratio of the contents of proand antiapoptotic proteins within them induced by severe hypoxia (SH) [14, 15]. Different PC regimes (number of episodes, duration of episodes) have been found to have effects with different effi cacies on the intracellular protection mechanisms. Further studies seeking optimum PC regimes, inducing effective mobilization of protective mechanisms, especially those involved in regulating apoptosis, are needed [1]. The aim of the present work was to study the effects of various PC regimes using MHH on the expression of the antiapoptotic protein Bcl-2 in neocortical and hippocampal neurons during and after exposure to harmful SH. Changes in the Expression of Antiapoptotic Protein Bcl-2 in the Rat Neocortex and Hippocampus in Different Hypobaric Hypoxia Regimes