AI Article Synopsis
- Hypothyroidism may help with recovery from brain injuries caused by lack of blood flow, but finding a way to benefit from it without negative side effects is a challenge.
- Researchers hypothesize that using a specific inhibitor can create a brain-focused reduced metabolism that protects against damage during such injuries, without disrupting overall thyroid hormone levels.
- Experiments in rats showed that this treatment significantly lowered brain injury markers and improved neuron survival, suggesting this method could be a new therapeutic strategy for minimizing damage from strokes.
Article Abstract
Hypothyroidism has been associated with better recovery from cerebral ischemia-reperfusion (IR) injury in humans. However, any therapeutic advantage of inducing hypothyroidism for mitigating IR injury without invoking the adverse effect of whole body hypothyroidism remains a challenge. We hypothesize that a deiodinase II (D2) inhibitor reverse triiodothyronine (rT3) may render brain specific hypometabolic state to ensue reduced damage during an acute phase of cerebral ischemia without affecting circulating thyroid hormone levels. Preclinical efficacy of rT3 as a neuroprotective agent was determined in rat model of middle cerebral artery occlusion (MCAO) induced cerebral IR and in oxygen glucose deprivation/reoxygenation (OGD/R) model in vitro. rT3 administration in rats significantly reduced neuronal injury markers, infarct size and neurological deficit upon ischemic insult. Similarly, rT3 increased cellular survival in primary cerebral neurons under OGD/R stress. Based on our results from both in vivo as well as in vitro models of ischemia reperfusion injury we propose rT3 as a novel therapeutic agent in reducing neuronal damage and improving stroke outcome.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212030 | PMC |
| http://dx.doi.org/10.1016/j.bbrc.2018.10.031 | DOI Listing |
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