Thyroid hormone (TH) is essential for normal brain development and may also promote recovery and neuronal regeneration after brain injury. TH acts predominantly through the nuclear receptors, TH receptor alpha (THRA) and beta (THRB). Additional factors that impact TH action in the brain include metabolism, activation of thyroxine (T4) to triiodothyronine (T3) by the enzyme 5'-deiodinase Type 2 (Dio2), inactivation by the enzyme 5-deiodinase Type 3 (Dio3) to reverse T3 (rT3), which occurs in glial cells, and uptake by the Mct8 transporter in neurons. Traumatic brain injury (TBI) is associated with inflammation, metabolic alterations and neural death. In clinical studies, central hypothyroidism, due to hypothalamic and pituitary dysfunction, has been found in some individuals after brain injury. TH has been shown, in animal models, to be protective for the damage incurred from brain injury and may have a role to limit injury and promote recovery. Although clinical trials have not yet been reported, findings from in vitro and in vivo models inform potential treatment strategies utilizing TH for protection and promotion of recovery after brain injury.

中文翻译：

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甲状腺激素和大脑：脑损伤后发育的作用机制以及在保护和促进恢复中的作用。

甲状腺激素（TH）对于正常的大脑发育必不可少，并且还可促进脑损伤后的恢复和神经元再生。TH主要通过核受体TH受体α（THRA）和β（THRB）起作用。影响大脑TH作用的其他因素包括新陈代谢，2'酶5'-脱碘酶（Dio2）激活甲状腺素（T4）到三碘甲甲状腺素（T3），5'-脱碘酶3（Dio3）的酶失活以逆转。 T3（rT3）发生在神经胶质细胞中，并被神经元中的Mct8转运蛋白摄取。颅脑外伤（TBI）与炎症，代谢改变和神经死亡有关。在临床研究中，在一些脑损伤后的个体中发现了由于下丘脑和垂体功能障碍引起的中枢性甲状腺功能减退症。在动物模型中已显示出TH 保护因脑损伤而引起的损伤，并可能起到限制损伤和促进恢复的作用。尽管尚未进行临床试验的报道，但体外和体内模型的发现为利用TH来保护和促进脑损伤后恢复的潜在治疗策略提供了参考。