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The delayed protective effect of GK-2, а dipeptide mimetic of Nerve Growth Factor, in a model of rat traumatic brain injuryстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 26 декабря 2018 г.
- Авторы: Genrikhs Elisaveta E., Voronkov Dmitriy N., Kapkaeva Marina R., Gudasheva Tatyana A., Glibka Yuliya A., Isaev Nickolay K., Stelmashook Elena V.
- Журнал: Brain Research Bulletin
- Том: 140
- Год издания: 2018
- Издательство: Elsevier BV
- Местоположение издательства: Netherlands
- Первая страница: 148
- Последняя страница: 153
- DOI: 10.1016/j.brainresbull.2018.05.002
- Аннотация: The delayed protective effect of GK-2, a dipeptide mimetic of Nerve Growth Factor, was investigated on the model of focal one-sided traumatic brain injury (TBI) of the sensorimotor cortex region on the 180th day after the injury. TBI caused a reliably disruption of the functions of the limbs contralateral to injury focus. The intraperitoneal administration of GK-2 (1 mg/kg) from 1st to 4th and from 7th to 10th days after TBI reduced the impairment of the motor functions of the limbs. This therapeutic effect significant manifested itself from the 7th day and continued until the end of the experiment – on the 180th day after TBI. Morphological studies of the animal brains on the 180th day after TBI demonstrated a decrease in the number of neurons in the V layer of the cerebral cortex and a decrease in the thickness of the corpus callosum. The treatment of animals with GK-2 after TBI statistically significant prevented a decrease in the density of neurons in the ipsilateral hemisphere and a decrease in the thickness of the corpus callosum in the contralateral hemisphere in comparison with untreated animals. Additionally, we showed in vitro that GK-2 exhibits neuroprotective properties under oxidative stress in primary hippocampal cultures. Our results demonstrate that the use of GK-2 at the early stages of development of traumatic brain damage can prevent such delayed damage as neuronal and axonal degeneration as well as reduce TBI-related disruptions of brain functions.
- Добавил в систему: Исаев Николай Константинович