Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury: Protective effects of the Mitochondria-Targeted Antioxidative Peptide SS-31

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Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury : Protective effects of the Mitochondria-Targeted Antioxidative Peptide SS-31

Czigler, Andras (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary

Toth, Luca (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary

Szarka, Nikolett (författare): Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary

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Berta, Gergely (författare): Medical Biology and University of Pecs, Medical School, Pecs, Hungary

Amrein, Kriszitina (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary

Czeiter, Endre (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Immunology and Biotechnology, University of Pecs, Medical School, Pecs, Hungary

Lendvai-Emmert, Dominika (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary

Bodo, Kornelia (författare): Immunology and Biotechnology, University of Pecs, Medical School, Pecs, Hungary

Tarantini, Stefano (författare): Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA

Koller, Akos (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Department of Morphology and Physiology, Semmelweis University, Budapest, Hungary; Sport-Physiology Research Center, University of Physical Education, Budapest, Hungary; Department of Physiology, New York Medical College, Valhalla, New York, USA

Ungvari, Zoltan (författare): Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA

Büki, Andras, 1966- (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary

Toth, Peter (författare): Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary

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Mary Ann Liebert, 2019
2019
Engelska.
Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 36:23, s. 3309-3315

Relaterad länk:: https://www.ncbi.nlm...; visa fler...; https://urn.kb.se/re...; https://doi.org/10.1...; visa färre...

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Traumatic brain injury (TBI) induces cerebrovascular oxidative stress, which is associated with neurovascular uncoupling, autoregulatory dysfunction, and persisting cognitive decline in both pre-clinical models and patients. However, single mild TBI (mTBI), the most frequent form of brain trauma, increases cerebral generation of reactive oxygen species (ROS) only transiently. We hypothesized that comorbid conditions might exacerbate long-term ROS generation in cerebral arteries after mTBI. Because hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive and spontaneously hypertensive rats (SHR) and assessed changes in cytoplasmic and mitochondrial superoxide (O2-) production by confocal microscopy in isolated middle cerebral arteries (MCA) 2 weeks after mTBI using dihydroethidine (DHE) and the mitochondria-targeted redox-sensitive fluorescent indicator dye MitoSox. We found that mTBI induced a significant increase in long-term cytoplasmic and mitochondrial O2- production in MCAs of SHRs and increased expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit Nox4, which were reversed to the normal level by treating the animals with the cell-permeable, mitochondria-targeted antioxidant peptide SS-31 (5.7 mg kg-1 day-1, i.p.). Persistent mTBI-induced oxidative stress in MCAs of SHRs was significantly decreased by inhibiting vascular NADPH oxidase (apocyinin). We propose that hypertension- and mTBI-induced cerebrovascular oxidative stress likely lead to persistent dysregulation of cerebral blood flow (CBF) and cognitive dysfunction, which might be reversed by SS-31 treatment.

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Av författaren/redakt...: Czigler, Andras; Toth, Luca; Szarka, Nikolett; Berta, Gergely; Amrein, Krisziti ...; Czeiter, Endre; visa fler...; Lendvai-Emmert, ...; Bodo, Kornelia; Tarantini, Stefa ...; Koller, Akos; Ungvari, Zoltan; Büki, Andras, 19 ...; Toth, Peter; visa färre...

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MEDICIN OCH HÄLSOVETENSKAP: MEDICIN OCH HÄLS ...; och Klinisk medicin; och Neurologi

Artiklar i publikationen: Journal of Neuro ...

Av lärosätet: Örebro universitet

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Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury : Protective effects of the Mitochondria-Targeted Antioxidative Peptide SS-31

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