ReferenceID 497
Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury
Pharmacol Res
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 exacerba
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- Reference Id
- 497
- Evidence Id
- 17087
- Core Evidence Id
- 17087
- Source Reference Id
- 965
- Herb2 Reference Id
- HBREF001675
- Subject Paper Key
- HBIN007532_23313345
- Pubmed Id
- 23313345
- Doi
- 10.1016/j.phrs.2012.12.009
- Paper Title
- Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury
- Paper 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.
- Journal
- Pharmacol Res
- Publish Year
- 2013
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Traumatic Brain Injury
- Paper Title Cn
- Paper Title En
- Exogenous T3 administration provides neuroprotection in a murine model of traumatic brain injury
- Bilingual Status
- semi_complete