The article deals with the current problem of neonatology and pediatric neurology — the issues of early diagnosis of perinatal hypoxic-ischemic brain injury in newborns, particularly, in prematurely born children. The work considers modern literature data on the mechanisms of hypoxic-ischemic perinatal brain damage. New data on the functioning, injury, as well as the mechanism of cell death of neuronal and glial origin in the developing brain are presented. It was shown that excitotoxicity (glutamatergic system), oxidative stress and aseptic inflammation are involved in the realization of this mechanism, the final result of which is cell death by necrosis and pathological apoptosis. It was emphasized that in immature neuronal tissue, the death of neurons occurs not only by the above paths, but also due to the combined necrotic-apoptotic (necroptotic) mechanism. The ambiguous role of glutamate receptors in the developing brain is analyzed. Literature data are presented that excitotoxicity, oxidative stress and inflammation against the background of peculiarities mitochondrial functioning in the brain lead to the onset of pathological apoptosis. It has been determined that the most promising in the early diagnosis of hypoxic-ischemic damage to the central nervous system in newborns, in particular premature babies, is the study of the level of neuron-specific proteins and antibodies to them, as well as proteins associated with the plasma membrane — intercellular adhesion molecules. The article analyzes the role of neuronal and glial markers, in particular glial fibrillary acidic protein, ubiquitin C-terminal hydrolase L1, myelin basic protein, as well as the role of pro-inflammatory cytokines in the mechanisms of damage to cells of the developing brain. The role of the membrane protein of cerebral capillary endotheliocytes, an intercellular adhesion molecule 1, as one of the markers of damage to the blood-brain barrier cells in various pathological processes, in particular hypoxia and ischemia, was determined.
Role of caspases, calpain and cdk5 in ammonia-induced cell death in developing brain cells
