Abstract
Subarachnoid hemorrhage (SAH) is a severe neurological disease, which is associated with a significant number of cases of premature mortality and disability worldwide. Mild hypothermia (MH) has been proposed as a potential therapeutic strategy to reduce neuronal injury following SAH. The present study aimed to investigate the mechanisms of MH's protective role in the process of SAH. The present study demonstrated that MH was able to protect against early brain injury in a rat model of SAH. Treating SAH rats with MH reduced the release of reactive oxygen species and prevented activation of apoptotic cascades. Furthermore, the protective effects of MH were shown to be mediated by enhanced activity of the tropomyosin receptor kinaseB/extracellular signal‑regulated kinases/cAMP response element binding protein (TrkB/ERK/CREB) pathway. Inhibition of TrkB/ERK/CREB activity using a small molecule inhibitor largely abolished the beneficial effects of MH in SAH rats. These results outline an endogenous mechanism underlying the neuroprotective effects of MH in SAH.
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