Chondroprotectors as modulators of neuroinflammation

Torshin, I. Yu.; Gromova, О. А.; Nazarenko, A G

doi:10.14412/2074-2711-2023-1-110-118

Cited by 2 publications

(1 citation statement)

References 38 publications

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“…Подавляющее число хронических заболеваний головного мозга тесно связано со снижением гемоперфузии, которая запускает ряд клеточных механизмов: нейродегенерацию [1], некроз и апоптоз нейронов [2], активацию и гибель астроцитов [3] и олигодендроглиоцитов, микроглиальную и астроглиальную активацию, повреждение гемато-энцефалического барьера [4], нарушение гемореологии и гемомикроциркуляции, эндотелиальную дисфункцию, окислительный стресс [5], нейровоспаление, приводящее к снижению когнитивных способностей [6]. Исследования В.Н.…”

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Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Gaivoronskii,

Chrishtop,

Nikonorova

et al. 2023

Bulletin of the Russian Military Medical Academy

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Cerebral hypoperfusion, as the main mechanism of age-associated diseases, is widespread, which leads to decreased work capacity in the most qualified segment of employees. The study aimed to analyze compensatory and adaptive reactions of the cerebral cortex, thyroid gland, and blood in cerebral hypoperfusion and its combination with short-term physical activity. Chronic cerebral hypoperfusion was modeled by permanent bilateral occlusion of the common carotid arteries. The study included 280 rats, of which 112 were subjected to daily short-term swimming as a model of rehabilitation measures. On days 1, 6, 8, 14, 21, 28, 35, 60, and 90 after surgery, the animals were subjected to the Morris water maze and open field tests. Histological sections of the brain and thyroid gland were examined. The concentrations of the active products of thiobarbituric acid, nitrites, and L-arginine in blood plasma were measured. The results showed that changes in the cerebral cortex and thyroid gland in the cerebral hypoperfusion model were characterized by a general stage: days 18, hypothyroid condition and death of cortical cells, cerebral hemispheres, predominantly neurons; weeks 23, stabilization, transition to the euthyroid condition, accompanied with thyrocyte desquamation, folliculogenesis, perifollicular hemocapillaries fullness, decreased functional activity of neurons, and astrocyte activation; weeks 45, incomplete adaptation, which is characterized by neurons approaching the vessels of the hemocirculatory channel and satellites sinking into the cytoplasm of neurons. Mosaicism of thyroid blood filling was also observed. After 3 months, degenerative changes in the cells of the cerebral cortex of the cerebral hemispheres appear, including a decrease in the numerical density of neurons and immunoreactive cells of glial fibrillar acid protein and a hyperthyroid state with signs of decompensation: plasmorrhagia and desquamation of the thyroid epithelium. Daily 15-min exercise with cerebral hypoperfusion demonstrated a neuroprotective effect, slowed down the progression of hypoxic and neurodegenerative changes, and reduced the concentration of nitrites and malondialdehyde in the blood and the levels of neuronal nitric oxide synthase in immunoreactive neurons.

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Section: Introductionunclassified

Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Gaivoronskii,

Chrishtop,

Nikonorova

et al. 2023

Bulletin of the Russian Military Medical Academy

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Molecular mechanisms of the effect of standardized placental hydrolysate peptides on mitochondria functioning

Torshin,

Gromova,

Tikhonova

et al. 2023

Terapevticheskii arkhiv

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Background. Human placenta hydrolysates (HPH), the study of which was initiated by the scientific school of Vladimir P. Filatov, are currently being investigated using modern proteomic technologies. HPH is a promising tool for maintaining the function of mitochondria and regenerating tissues and organs with a high content of mitochondria (liver, heart muscle, skeletal muscles, etc.). The molecular mechanisms of action of HPH are practically not studied. Aim. Identification of mitochondrial support mitochondrial function-supporting peptides in HPH (Laennec, produced by Japan Bioproducts). Materials and methods. Data on the chemical structure of the peptides were collected through a mass spectrometric experiment. Then, to establish the amino acid sequences of the peptides, de novo peptide sequencing algorithms based on the mathematical theory of topological and metric analysis of chemographs were applied. Bioinformatic analysis of the peptide composition of HPH was carried out using the integral protein annotation method. Results. The biological functions of 41 peptides in the composition of HPH have been identified and described. Among the target proteins, the activity of which is regulated by the identified peptides and significantly affects the function of mitochondria, are caspases (CASP1, CASP3, CASP4) and other proteins regulating apoptosis (BCL2, CANPL1, PPARA), MAP kinases (MAPK1, MAPK3, MAPK4, MAPK8, MAPK9 , MAPK10, MAPK14), AKT1/GSK3B/MTOR cascade kinases, and a number of other target proteins (ADGRG6 receptor, inhibitor of NF-êB kinase IKKE, pyruvate dehydrogenase 2/3/4, SIRT1 sirtuin deacetylase, ULK1 kinase). Conclusion. HPH peptides have been identified that promote inhibition of mitochondrial pore formation, apoptosis, and excessive mitochondrial autophagy under conditions of oxidative/toxic stress, chronic inflammation, and/or hyperinsulinemia.

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Chondroprotectors as modulators of neuroinflammation

Cited by 2 publications

References 38 publications

Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Molecular mechanisms of the effect of standardized placental hydrolysate peptides on mitochondria functioning

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