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Biomedical subjects

L V Cherkasova

Publications and source records attributed to L V Cherkasova.

At least 19 recordsLinked to original sources

Normalization of protein synthesis in dystrophic neurons of cerebral cortex in rats after hypoxia, opening of the blood-brain barrier and treatment with organospecific RNA.

The possibility of normalization of protein synthesis intensity was explored in dystrophic neurons and in the total brain cortex of rats after acute hypoxic hypoxia. We avoided transplantation of embryonic nervous tissue (ENT) into the rat brain, as we did before, as well as operations and brain damages in opening of the blood-brain barrier (BBB) caused by hypoxia and intramuscular injections of organo (brain)-specific RNA. As shown by the autoradiographic and biochemical methods using radioactive isotopes (3H-leucine), hypoxia causes a statistically significant reduction in the intensity of protein synthesis which increases and becomes normalized after injection of brain-specific RNA into femoral muscles of animals. Thus, it is possible to normalize hypoxia-inhibited compensation-restoration processes in the brain cortex of animals and, probably, the function of the higher nervous activity using the new simple and harmless biological method. The data presented are of priority significance and important both for development of a number of fundamental biological problems and for medicine since the described method permits the treatment of some serious nervous and mental diseases in humans.

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Normalization of protein synthesis and the structure of brain dystrophic neurons after the action of hypoxia, 10% NaCl and organ-specific RNA.

It was shown previously (Polezhaev and Alexandrova, 1986) that hypoxic hypoxia causes mass (up to 30%) diffuse dystrophy of brain cortex and hippocamp neurons in rats, disturbances in the higher nervous activity, reduction of protein, RNA synthesis in neurons and of DNA synthesis in the whole brain cortex. Transplantation of embryonic nervous tissue (ENT) in one of the hemispheres normalizes all the above abnormalities observed in some neurologic and mental diseases in humans. However, transplantation may entail injuries of parenchyma and brain blood vessels. This forces researchers to search for another biological method similar by its action but safer and simpler. ENT transplantation has a dual action: 1) formation of biologically active substances (BAS) releasing from the ENT transplant and from the host brain nervous tissue upon operation; 2) establishment of synaptic connections between the transplant and host neurons. Previously we (Vitvitsky, 1987) described the isolation of BAS from rat forebrain in the form of organ-specific RNA. The latter was injected intraperitoneally several times to post-hypoxic rats in which 30 min prior to that the blood-brain barrier (BBB) was opened by injecting intravenously and intraperitoneally 10% NaCl solution without damaging the host brain. At the beginning 10% NaCl increased the destruction of brain cortical neurons and then stimulated protein synthesis in them. RNA injections stimulated the synthesis in cortical neurons and normalized their structure. Thus, we propose a safe and simple method for normalization of dystrophic neurons which can be used after certain improvement for curing neurodegenerative and neuropsychic diseases in humans.

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Stimulation of protein synthesis in dystrophic brain cortex neurons of hypoxia-subjected rats by proliferation-activating protein isolated from nervous tissue of newborn animals.

Hypoxia causes mass diffuse dystrophy of brain cortex neurons, reduces RNA and protein synthesis in neurons and DNA synthesis in the total brain cortex in adult rats. Subsequent transplantation of embryonic nervous tissue (ENT) into the brain of hypoxia-subjected rats normalizes the structure of a considerable part of dystrophic neurons. A protein activator (molecular mass 30,000 D and PI 6.8) was isolated from intensively proliferating cerebellum tissue of newborn rats, dissolved in physiological solution, and injected into one of the hemispheres of hypoxia-subjected rats. The activator significantly stimulated the proliferation of recipient brain cells and normalized the protein biosynthesis in cortical neurons of the recipients like an ENT transplant. Injection into the brain of hypoxia-subjected rats of a physiological solution alone does not produce such an effect. The presented results have been obtained by the methods of autoradiography and biochemistry using 3H-leucine for estimating the intensity of protein synthesis by its incorporation into cells.

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Stimulation of RNA synthesis in brain cortex of rats after hypoxia by transplantation of embryonic nervous tissue.

Our early studies (Polezhaev and Alexandrova, 1986) have shown that acute hypoxic hypoxia in rats causes mass (up to 36%) diffuse dystrophy of brain cortex neurons and that after transplantation of embryonic nervous tissue (ENT) into the brain of hypoxia-exposed rats the dystrophy and death of cortical neurons are reduced to 25% due to normalization of a part of dystrophic neurons. In the present work we studied changes in the RNA synthesis in neurons and in the total brain cortex of rats after hypoxia and subsequent transplantation of ENT into their brain by the autoradiographic and biochemical methods using 14C-adenine. It has been shown that under the action of hypoxia the RNA synthesis in neurons and in the total brain cortex of rats is reduced and after transplantation of ENT into the brain of these rats the RNA synthesis is stimulated and normalized both in neurons and in the total brain cortex.

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Normalization of protein synthesis in brain cortex of rats after hypoxia by transplantation of embryonic nervous tissue.

It has been shown autoradiographically using 3H-lysine-3H-glycin mixture that acute hypoxic hypoxia leading to mass diffuse dystrophy of brain cortex neurons in rats causes a statistically significant decrease in the level of protein synthesis in cortical neurons. The biochemical study of the same material using 3H-leucine has demonstrated that the overall level of protein synthesis in the total cortical tissue (in nerve and non-nerve cells) is not reduced after hypoxia probably due to a high resistance of glial and other non-nerve cells to oxygen deficiency. Transplantation of embryonic nervous tissue into the brain of rats exposed to hypoxia results not only in normalization of the structure of a part of dystrophic neurons but also in a statistically significant increase in the level of protein synthesis which is retained up to the end of the experiment (i. e. for 120 days following the operation) in the total cortical tissue and reaches the normal value in neurons as established autoradiographically.

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Changes of DNA synthesis in brain cortical cells after transplantation of embryonic nervous tissue into the brain of rats after hypoxia.

Autoradiographic and biochemical studies with 3H-thymidine have shown that after transplantation of embryonic nervous tissue of rats into the brain of adult rats, intact and subjected to acute hypoxic hypoxia causing mass dystrophy of neurons in the brain cortex of recipients, there occurs stimulation of DNA synthesis in non-nerve cells: glial cells, macrophages and endothelial cells. Stimulation is much more pronounced in the operated hemisphere than in the non-operated one and in intact rats than in hypoxia-subjected ones. On the whole, DNA synthesis was not observed in brain nerve cells except individual neurons located near the wound canal and the transplant.

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Transplantation of dissociated embryonic brain cells in the brain of adult normal rats and rats subjected to hypoxia.

3H-thymidine-labelled dissociated brain cells of rat embryos were implanted in the brain of adult normal and hypoxia-subjected rats. In both cases these cells survived successfully, differentiated into neurons and glial cells and remained viable throughout the whole experimental period (60 days). These cells were able to synthesize DNA and divide. Dissociated cells of rat embryo brains tended to aggregate after transplantation and were present not only as single neurons but also as large neuronal assemblies having the shape of islets and columns. These cells promoted considerable normalization of degenerated rat cortical neurons after hypoxia.

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