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Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury
Author(s) -
Paterniti Irene,
Crupi Rosalia,
Campolo Michela,
Di Paola Rosanna,
Cuzzocrea Salvatore,
Esposito Emanuela
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1177.8
Subject(s) - traumatic brain injury , neuroprotection , neuroinflammation , medicine , glial fibrillary acidic protein , neurodegeneration , microglia , nitric oxide synthase , neurotrophic factors , endocrinology , pharmacology , neuroscience , nitric oxide , inflammation , biology , immunohistochemistry , receptor , disease , psychiatry
Traumatic brain injury (TBI) induces primary and secondary damage in both the endothelium and the brain parenchyma that exacerbates the initial injury. Controlled cortical impact injury (CCI) is a widely‐used model of TBI. Here, we used a mice model of experimental TBI, to determine whether 3,5,3′‐triiodothyronine (T3) attenuates post‐traumatic neurodegeneration and neuroinflammation. Treatment with T3 (100 μg/kg, i.p.) 1 hour after TBI resulted in a significant improvement of motor and cognitive recovery after CCI, as well as markedly reducing lesion volumes. Mouse model for brain injury showed an increase of glial fibrillary acidic protein, a marker of a reactive astrocytes, and formation of inducible nitric oxide synthase (iNOS). Western blot analysis revealed the ability of T3 to reduce brain trauma through modulation of cytoplasmic‐nuclear shuttling of nuclear factor‐κB (NF‐κB).Twenty‐four hrs after brain trauma,T3‐treated mice also showed significantly less number of TUNEL(+) apoptotic neurons and curtailed induction of Bax, compared to vehicle control. In addition, T3 significantly enhanced the post‐TBI expression of the neuroprotective neurotrophins (BDNF, and GDNF) compared to vehicle. Our data provide an additional mechanism for the anti‐inflammatory effects of thyroid hormone with critical implications in immunopathology at the cross‐roads of the immune‐endocrine circuits.