Email this article EFFECT OF KK1 PEPTIDE ON MAINTENANCE OF APOPTOSIS MARKERS IN RATS BRAIN CAUSED BY SEVERE CARBON OXIDE POISONING
- Authors: Tolkach P.G.1, Basharin V.A.1, Kolobov A.A.2, Rogovskaya N.Y.3, Babakov V.N.3
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Affiliations:
- S.M. Kirov Military Medical Academy, Ministry of Defense of the Russian Federation
- State Research Institute of High-pure Biopreparations, Federal Medical Biological Agency
- Research Institute of Hygiene, Occupational Pathology and Human Ecology, Federal Medical Biological Agency
- Issue: No 3 (2016)
- Pages: 10-14
- Section: Articles
- Published: 28.06.2016
- URL: https://rjsocmed.com/0869-7922/article/view/640943
- DOI: https://doi.org/10.36946/0869-7922-2016-3-10-14
- ID: 640943
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Abstract
Carbon oxide poisoning leads to the development of delayed CNS functions disturbances. These disturbances may be not only linked to the development of hemic hypoxia. In a number of research works, nonspecific neurotoxic carbon oxide mechanisms of action were described, one of which is activation of programmed cell death developing as apoptosis. One of the preparations having neuroprotective action mode is a synthetic analog sequence of adrenokortikotropic hormone – KK1 peptide. In this research, laboratory animals were exposed to acute heavy carbon oxide poisoning in a dose of 0.8 LC50 within 30 min. KK1 peptide was administrated intranasally in a dose of 40 mkg/kg/day within 5 days. In rats brain gomogenates, the maintenance of active forms of marker proteins associated with apoptosis early stages was investigated at different time after intoxication with carbon oxide. As a result of the conducted research, it was established that the use of KK1 peptide leads to the decrease of the maintenance of r53 protein active forms and Akt1 protein kinase on 7th and 14th days after a heavy poisoning with carbon oxide. Results of the experiment performed allow to suggest that at that type of pathology the potential mechanism of neuroprotective effect of synthetic KK1 tetrapeptide is connected with restricted development of apoptosis in brain.
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About the authors
P. G. Tolkach
S.M. Kirov Military Medical Academy, Ministry of Defense of the Russian Federation
Author for correspondence.
Email: noemail@neicon.ru
Russian Federation
V. A. Basharin
S.M. Kirov Military Medical Academy, Ministry of Defense of the Russian Federation
Email: noemail@neicon.ru
Russian Federation
A. A. Kolobov
State Research Institute of High-pure Biopreparations, Federal Medical Biological Agency
Email: noemail@neicon.ru
Russian Federation
N. Yu. Rogovskaya
Research Institute of Hygiene, Occupational Pathology and Human Ecology, Federal Medical Biological Agency
Email: noemail@neicon.ru
Russian Federation
V. N. Babakov
Research Institute of Hygiene, Occupational Pathology and Human Ecology, Federal Medical Biological Agency
Email: noemail@neicon.ru
Russian Federation
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