The Effect of Severe Hypobaric Hypoxia on the Content of the Autophagy Marker LC3 in the Hippocampus of Rats

Abstract

Autophagy is an intracellular mechanism of degradation of cytoplasmic molecules and organelles in autophagosomes, which is necessary for maintaining cellular homeostasis and normal functioning of neurons, both at rest and under the action of extreme factors. Despite this, the role of autophagy in the mechanisms of adaptive and pathological reactions of the brain is still poorly understood and is an important problem for research. The study of autophagy processes in neurons under conditions of damaging factors is of fundamental importance and, at the same time, can be useful in terms of the development of specific drugs aimed at the links of the autophagic cascade. Since one of the most common injurious factors is hypoxia, the aim of this work was to assess the activity of the autophagy process in the hippocampus of rats after exposure to severe hypoxia. The immunohistochemical method was used. It was revealed that severe hypobaric hypoxia (180-mm Hg, 3 h) increases the autophagy activity in neurons of the hippocampal fields. This is manifested by a decrease in the content of the LC3 marker 1 day after exposure. At the same time, 3 days after hypoxia, the LC3 level is restored to control values. Thus, the data that are obtained in the model in vivo indicate that the autophagic degradation is intensified in the hippocampus of rats in response to the action of hypobaric hypoxia.