Abstract
BDNF-Mediated Regulation of the Brain Mitochondria Functional State in Hypoxia
Highlights
Hypoxia is one of the leading factors of brain cell damage accompanying traumatic and ischemic processes
The aim of the study was to study the effect of TrkB-mediated action of the brain-derived neurotrophic factor on animal survival and activity of mitochondrial respiratory chain complexes I, II in acute hypobaric hypoxia model in vivo
All animals were divided into the following groups: group 1 — intact mice; group 2 — control animals exposed to acute hypobaric hypoxia without introduction of the examined substances; group 3 — mice exposed to acute hypobaric hypoxia with preventive intraperitoneal injection of selective blocker of TrkB receptors — ANA12 at a concentration of 0.5 mg/kg; group 4 — mice exposed to acute hypobaric hypoxia with preventive intranasal injection of brain-derived neurotrophic factor (BDNF) at a concentration of 4 mg/kg; group 5 — a comparison group of animals exposed to acute hypobaric hypoxia with preventive introduction of 1% dimethyl sulfoxide (DMSO) in combination with Tween 20 to exclude the influence
Summary
Hypoxia is one of the leading factors of brain cell damage accompanying traumatic and ischemic processes. Increased sensitivity of the brain tissue to oxygen deficiency is determined by great energy consumption necessary for its functioning. Reduction of oxygen concentration causes derangements in the electron transport function of their respiratory chain and is a phase process (Figure 1). These damages are non-specific as they always start in the area of mitochondrial enzyme complex I (NAD-dependent area of the respiratory chain) and involve thereafter the area of cytochromes B, C and cytochrome oxidase [1,2,3,4,5,6,7,8]. In spite of the variety of medicines, antihypoxants, there are different limitations for their use in brain pathologies because of a great number of
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