Abstract
Enhancement of astrocyte metabolism in mice significantly decreases lesion size after stroke. This was achieved after purinergic stimulation, but we know that thyroid hormones (TH) can also increase mitochondrial metabolism. Acute treatment with triiodothyronine (T3) increases long‐chain fatty acid oxidation (FAO) in several tissues to improve metabolism. Because astrocytes also use fatty acids for energy, we hypothesized that THs increase astrocyte FAO and improve survival after oxidative stress or stroke.ResultsNanomolar concentrations of either diiodothyronine (T2) or T3 increase astrocyte FAO of [3H]palmitate into 3H2O by over 30% (p<0.01). The astrocyte mitochondrial membrane potential was measured using the potential sensitive dye tetramethyl rhodamine methyl ester. Acute T2 treatment (15 minutes) tripled the dye intensity (p<0.05), indicating improved mitochondrial membrane potential. These data are consistent with increased energy production upon TH treatment. Astrocytes were stressed with hydrogen peroxide, and viability was measured using the vital dye calcien‐AM. T2 and T3 each increased astrocyte viability 25% (p<0.01). To test if TH is protective in vivo, we induced focal ischemia in mice. Administration of T2 decreased the necrotic volume in the brain by half (p=0.02) 24 hours post‐stroke. Future testing will determine if TH‐mediated survival of astrocytes is dependent on FAO.
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