Involvement of Renin-Angiotensin system (RAS) components in mild traumatic brain injury.

Autor: Machado CA; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil. Electronic address: carolineamachado@gmail.com., Oliveira BDS; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., de Barros JLVM; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., Fernandes HB; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., de Brito Toscano EC; Department of Pathology, Federal University of Juiz de Fora (UFJF) Medical School, Juiz de Fora, Brazil., Kangussu LM; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., Guimarães PPG; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais., Simões E Silva AC; Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., Teixeira AL; The Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, Lozano Long School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA., de Miranda AS; Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil; Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil. Electronic address: mirandaas@icb.ufmg.br.
Jazyk: angličtina
Zdroj: Brain research [Brain Res] 2025 Jan 01; Vol. 1846, pp. 149266. Date of Electronic Publication: 2024 Oct 05.
DOI: 10.1016/j.brainres.2024.149266
Abstrakt: The Renin Angiotensin System (RAS) plays a pathophysiological role in traumatic brain injury (TBI) but the evidence of its involvement in mild TBI (mTBI) is still limited. We aimed at investigating the levels of components from both the classical and counter-regulatory axis of the RAS in a mTBI animal model. Mice with mTBI displayed enhanced ACE/Ang II/AT 1 R axis ipsilateral- and contralaterally to the trauma in the hippocampus and prefrontal cortex during acute (24 and 72 h) and later (30 days) timepoints. Increase in Ang-(1-7) levels alongside reduction in Mas receptor expression in hippocampus and prefrontal cortex was also observed after injury. Conversely, mTBI-mice presented higher expression of AT 2 receptor in the contralateral hippocampus and the ipsilateral prefrontal cortex. Importantly, treatment with telmisartan, an AT 1 R blocker, and perindopril, an ACE inhibitor, were able to prevent mTBI-associated locomotor activity impairment and anxiety-like behavior, corroborating the involvement of RAS in the pathophysiology of mTBI. We provided original evidence that components of classical and alternative RAS axes undergo alterations in key brain areas following a mTBI in a time and hemisphere dependent manner. Our findings also open new avenues for investigating the therapeutic potential of RAS components in mTBI.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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