T3 alleviates neuroinflammation and reduces early brain injury after subarachnoid haemorrhage by promoting mitophagy via PINK 1-parkin pathway.

Subarachnoid haemorrhage (SAH) is a common and devastating complication of haemorrhagic stroke. SAH is characterised by high mortality rates, permanent disabilities, and is often caused by the rupture of intracranial aneurysms. Low serum triiodothyronine (T3) concentrations have been associated with severe SAH and poor prognosis. T3 has been previously described as an inhibitor of lung fibrosis, and it acts by stimulating autophagy and mitophagy. Here, we indicated in vitro that T3 treatment suppressed neuronal apoptosis by reducing the release of mitochondrial reactive oxygen species (ROS), leading to mitochondrial membrane potential (MMP) decrease. Moreover, this preventative effect was reversed by PINK 1-siRNA treatment. We showed that in vivo T3 treatment promoted mitophagy, decreased microglial activation, alleviated neuroinflammation, and reduced neuronal apoptosis following SAH. Overall, this thyroid hormone (TH) exerts a protective effect on neurones after SAH via the PINK 1/PARKIN pathway. Considering the protective function of TH against neuronal damage, further research can establish TH treatment as a promising and effective therapeutic option for early brain injury (EBI) after SAH.
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