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Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury.
Pharmacol Res. 2013 Apr; 70(1):80-9.PR

Abstract

Traumatic brain injury (TBI) induces primary and secondary damage in both the endothelium and the brain parenchyma. While neurons die quickly by necrosis, a vicious cycle of secondary injury in endothelial cells exacerbates the initial injury. Thyroid hormones are reported to be decreased in patients with brain injury. Controlled cortical impact injury (CCI) is a widely used, clinically relevant model of TBI. Here, using CCI in adult male mice, we set to determine whether 3,5,3'-triiodothyronine (T3) attenuates posttraumatic neurodegeneration and neuroinflammation in an experimental model of TBI. Treatment with T3 (1.2μg/100g body weight, i.p.) 1h after TBI resulted in a significant improvement in motor and cognitive recovery after CCI, as well as in marked reduction of lesion volumes. Mouse model for brain injury showed reactive astrocytes with increased glial fibrillary acidic protein, 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 hours after brain trauma, T3-treated mice also showed significantly lower 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.

Authors+Show Affiliations

Department of Biological and Environmental Sciences, University of Messina, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23313345

Citation

Crupi, Rosalia, et al. "Exogenous T3 Administration Provides Neuroprotection in a Murine Model of Traumatic Brain Injury." Pharmacological Research, vol. 70, no. 1, 2013, pp. 80-9.
Crupi R, Paterniti I, Campolo M, et al. Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury. Pharmacol Res. 2013;70(1):80-9.
Crupi, R., Paterniti, I., Campolo, M., Di Paola, R., Cuzzocrea, S., & Esposito, E. (2013). Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury. Pharmacological Research, 70(1), 80-9. https://doi.org/10.1016/j.phrs.2012.12.009
Crupi R, et al. Exogenous T3 Administration Provides Neuroprotection in a Murine Model of Traumatic Brain Injury. Pharmacol Res. 2013;70(1):80-9. PubMed PMID: 23313345.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury. AU - Crupi,Rosalia, AU - Paterniti,Irene, AU - Campolo,Michela, AU - Di Paola,Rosanna, AU - Cuzzocrea,Salvatore, AU - Esposito,Emanuela, Y1 - 2013/01/08/ PY - 2012/11/05/received PY - 2012/12/12/revised PY - 2012/12/26/accepted PY - 2013/1/15/entrez PY - 2013/1/15/pubmed PY - 2013/9/11/medline SP - 80 EP - 9 JF - Pharmacological research JO - Pharmacol. Res. VL - 70 IS - 1 N2 - Traumatic brain injury (TBI) induces primary and secondary damage in both the endothelium and the brain parenchyma. While neurons die quickly by necrosis, a vicious cycle of secondary injury in endothelial cells exacerbates the initial injury. Thyroid hormones are reported to be decreased in patients with brain injury. Controlled cortical impact injury (CCI) is a widely used, clinically relevant model of TBI. Here, using CCI in adult male mice, we set to determine whether 3,5,3'-triiodothyronine (T3) attenuates posttraumatic neurodegeneration and neuroinflammation in an experimental model of TBI. Treatment with T3 (1.2μg/100g body weight, i.p.) 1h after TBI resulted in a significant improvement in motor and cognitive recovery after CCI, as well as in marked reduction of lesion volumes. Mouse model for brain injury showed reactive astrocytes with increased glial fibrillary acidic protein, 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 hours after brain trauma, T3-treated mice also showed significantly lower 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. SN - 1096-1186 UR - https://www.unboundmedicine.com/medline/citation/23313345/Exogenous_T3_administration_provides_neuroprotection_in_a_murine_model_of_traumatic_brain_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-6618(13)00002-9 DB - PRIME DP - Unbound Medicine ER -