It feels as if I have posted more abstracts about uses of T3 other than for treating hypothyroidism. Almost feels as if every other specialty than endocrinology is aware, and becoming ever more aware, of the potential benefits of appropriate use of T3.
Perhaps the irony is especially strong with respect to head injury - which can itself lead to hypothyroidism due to damage to the pituitary, etc.
Pharmacol Res. 2013 Apr;70(1):80-9. doi: 10.1016/j.phrs.2012.12.009. Epub 2013 Jan 8.
Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury.
Crupi R1, Paterniti I, Campolo M, Di Paola R, Cuzzocrea S, Esposito E.
1 Department of Biological and Environmental Sciences, University of Messina, Italy.
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.
Copyright © 2013 Elsevier Ltd. All rights reserved.