IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)

Experimental traumatic brain injury (TBI) causes a stable stress response and changes the expression of various cytokine genes and neurotrophic factors. The goal of this study was to reveal changes in the levels of the corticosterone and testosterone hormones and the BDNF cytoki...

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Autores principales:	E. E. Fomicheva, S. N. Shanin, T. A. Filatenkova, N. B. Serebryanaya
Formato:	article
Lenguaje:	RU
Publicado:	SPb RAACI 2020
Materias:	experimental traumatic brain injury corticosterone testosterone bdnf ril-2 Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/cb6ffe2958e14c85b62dfdf987538dc1
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spelling	oai:doaj.org-article:cb6ffe2958e14c85b62dfdf987538dc12021-11-18T08:03:49ZIL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)1563-06252313-741X10.15789/1563-0625-IAR-1973https://doaj.org/article/cb6ffe2958e14c85b62dfdf987538dc12020-08-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/1973https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XExperimental traumatic brain injury (TBI) causes a stable stress response and changes the expression of various cytokine genes and neurotrophic factors. The goal of this study was to reveal changes in the levels of the corticosterone and testosterone hormones and the BDNF cytokine in blood serum, as well as the expression of the BDNF gene in hypothalamus in order to determine the opportunity of correcting the TBI damage with rIL-2. We used a rat model of “dropping load”: mild TBI was caused by falling of the 115 g load from the height of 80 cm, or 120 cm to produce a moderate-degree trauma. After TBI (immediately, or 72 hours later), the rats were injected daily with recombinant human interleukin-2 (Roncoleukin) at a dose of 30 μg/kg, a total of 3 injections. Control animals (also with TBI) received 0.15 M NaCl injections. Blood serum concentrations of corticosterone, testosterone, and BDNF were measured with ELISA tests. BDNF gene expression in hypothalamus was measured using RT-PCR. Results: the experiments showed a relationship between hormone concentrations and severity of head injury. In mild TBI, blood corticosterone levels reached a peak 2 hours after the injury, while in moderate TBI, the peak concentration of corticosterone was lower, being delayed in time (after 24 hours). Corticosterone and testosterone concentrations changed reciprocally in the both groups of injured animals. With injection of rIL-2 in both groups, corticosterone and testosterone levels were significantly increased. On day 7 after TBI, the BDNF level in blood serum was decreased, but it was raised in experimental group that received rIL-2. On day 7, the increase of BDNF gene expression in hypothalamus was more pronounced, when rIL-2 was administered at 72 hours after the head injury. The revealed positive association of BDNF levels and glucocorticoid hormones after mild TBI, like as possible coordination of these parameters with rIL-2 injection after experimental moderate TBI provides a reason to assume that the favorable impact of rIL-2 on the CNS recovery after TBI is, in part, mediated by the mutual modulating interaction of BDNF and glucocorticoid hormones.E. E. FomichevaS. N. ShaninT. A. FilatenkovaN. B. SerebryanayaSPb RAACIarticleexperimental traumatic brain injurycorticosteronetestosteronebdnfril-2Immunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 22, Iss 4, Pp 647-656 (2020)
institution	DOAJ
collection	DOAJ
language	RU
topic	experimental traumatic brain injury corticosterone testosterone bdnf ril-2 Immunologic diseases. Allergy RC581-607
spellingShingle	experimental traumatic brain injury corticosterone testosterone bdnf ril-2 Immunologic diseases. Allergy RC581-607 E. E. Fomicheva S. N. Shanin T. A. Filatenkova N. B. Serebryanaya IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
description	Experimental traumatic brain injury (TBI) causes a stable stress response and changes the expression of various cytokine genes and neurotrophic factors. The goal of this study was to reveal changes in the levels of the corticosterone and testosterone hormones and the BDNF cytokine in blood serum, as well as the expression of the BDNF gene in hypothalamus in order to determine the opportunity of correcting the TBI damage with rIL-2. We used a rat model of “dropping load”: mild TBI was caused by falling of the 115 g load from the height of 80 cm, or 120 cm to produce a moderate-degree trauma. After TBI (immediately, or 72 hours later), the rats were injected daily with recombinant human interleukin-2 (Roncoleukin) at a dose of 30 μg/kg, a total of 3 injections. Control animals (also with TBI) received 0.15 M NaCl injections. Blood serum concentrations of corticosterone, testosterone, and BDNF were measured with ELISA tests. BDNF gene expression in hypothalamus was measured using RT-PCR. Results: the experiments showed a relationship between hormone concentrations and severity of head injury. In mild TBI, blood corticosterone levels reached a peak 2 hours after the injury, while in moderate TBI, the peak concentration of corticosterone was lower, being delayed in time (after 24 hours). Corticosterone and testosterone concentrations changed reciprocally in the both groups of injured animals. With injection of rIL-2 in both groups, corticosterone and testosterone levels were significantly increased. On day 7 after TBI, the BDNF level in blood serum was decreased, but it was raised in experimental group that received rIL-2. On day 7, the increase of BDNF gene expression in hypothalamus was more pronounced, when rIL-2 was administered at 72 hours after the head injury. The revealed positive association of BDNF levels and glucocorticoid hormones after mild TBI, like as possible coordination of these parameters with rIL-2 injection after experimental moderate TBI provides a reason to assume that the favorable impact of rIL-2 on the CNS recovery after TBI is, in part, mediated by the mutual modulating interaction of BDNF and glucocorticoid hormones.
format	article
author	E. E. Fomicheva S. N. Shanin T. A. Filatenkova N. B. Serebryanaya
author_facet	E. E. Fomicheva S. N. Shanin T. A. Filatenkova N. B. Serebryanaya
author_sort	E. E. Fomicheva
title	IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
title_short	IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
title_full	IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
title_fullStr	IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
title_full_unstemmed	IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)
title_sort	il-2 and regulation of stress hormones and bdnf neurotropic factor levels after experimental traumatic brain injury (tbi)
publisher	SPb RAACI
publishDate	2020
url	https://doaj.org/article/cb6ffe2958e14c85b62dfdf987538dc1
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IL-2 and regulation of stress hormones and BDNF neurotropic factor levels after experimental traumatic brain injury (TBI)

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