Lv Ou, Zhou Fenggang, Zheng Yongri, Li Qingsong, Wang Jianjiao, Zhu Yulan
Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Mol Med Rep. 2016 Oct;14(4):3901-7. doi: 10.3892/mmr.2016.5709. Epub 2016 Sep 5.
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 kinase B/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.
蛛网膜下腔出血（SAH）是一种严重的神经系统疾病，在全球范围内与大量过早死亡和残疾病例相关。亚低温（MH）已被提出作为一种潜在的治疗策略，以减少SAH后的神经元损伤。本研究旨在探讨MH在SAH过程中的保护作用机制。本研究表明，MH能够在SAH大鼠模型中预防早期脑损伤。用MH治疗SAH大鼠可减少活性氧的释放，并防止凋亡级联反应的激活。此外，MH的保护作用被证明是由原肌球蛋白受体激酶B/细胞外信号调节激酶/cAMP反应元件结合蛋白（TrkB/ERK/CREB）途径的活性增强介导的。使用小分子抑制剂抑制TrkB/ERK/CREB活性在很大程度上消除了MH对SAH大鼠的有益作用。这些结果概述了MH在SAH中神经保护作用的内源性机制。
