The involvement of thyroid hormones and related molecules in neuroprotective mechanisms in the developing brain.

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Neonatal hypoxic〓ischemic encephalopathy (HIE) is one of the major causes of neurodegeneration and mortality in the neonatal period. Although hypoxic preconditioning (HPC) provided strong neuroprotection against HIE in an animal model, the mechanism underlying this effect is not fully understood especially in the immature brain. Here, we investigated whether thyroid hormones (THs), which are essential during normal brain development, contribute to the neuroprotective mechanisms of HPC by using an established model of HPC in neonatal rats. HPC treatment (8% O2 for 2.5 h at 37°C) was performed in immature rats at postnatal day6 (P6). Subsequently, we investigated the levels of THs, TH receptors (TRs) and type2 and 3 deiodinases (D2 and D3) mRNA, and myelin basic protein (MBP) at 24 h after HPC treatment at P7. The local level of triiodothyronine (T3) was upregulated 24 h after HPC treatment in the developing rat brain, probably via the upregulation of D2. In addition, the expression of MBP, which is the downstream protein of T3, was significantly increased 24 h after HPC treatment. The present study indicates that thyroid hormones and their associated molecules may play a significant role in neuroprotective mechanisms during the developmental period.