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亚低温通过激活细胞外信号调节激酶信号通路保护蛛网膜下腔出血早期脑损伤大鼠模型中神经元自噬的增加。

Moderate hypothermia protects increased neuronal autophagy via activation of extracellular signal-regulated kinase signaling pathway in a rat model of early brain injury in subarachnoid hemorrhage.

机构信息

College of Clinical Medicine, North China University of Science and Technology, Tangshan, 063000, PR China; Department of Neurosurgery, Affiliated Hospital of North China University of Science and Technology, Tangshan, 063000, PR China.

College of Clinical Medicine, North China University of Science and Technology, Tangshan, 063000, PR China.

出版信息

Biochem Biophys Res Commun. 2018 Jul 20;502(3):338-344. doi: 10.1016/j.bbrc.2018.05.158. Epub 2018 May 30.

Abstract

Moderate hypothermia (MH) used as treatment for neurological diseases has a protective effect; however, its mechanism remains unclear. Neuronal autophagy is a fundamental pathological process of early brain injury in subarachnoid hemorrhage (SAH). We found that moderate activation of autophagy can reduce nerve cells damage. In this study, We found that MH can moderately increase the level of autophagy in nerve cells and improve the neurological function in rats. This type of autophagy activation is dependent on extracellular signal-regulated kinase (ERK) signaling pathways. The level of neuronal autophagy was down-regulated significantly by using U0126, an ERK signaling pathway inhibitor. In summary, these results suggest that MH can moderately activate neuronal autophagy through ERK signaling pathway, reduce nerve cell death, and produce neuroprotective effects.

摘要

亚低温(MH)作为治疗神经疾病的一种方法具有保护作用;然而,其机制尚不清楚。神经元自噬是蛛网膜下腔出血(SAH)早期脑损伤的基本病理过程。我们发现适度激活自噬可以减少神经细胞损伤。在这项研究中,我们发现 MH 可以适度增加神经细胞中的自噬水平,改善大鼠的神经功能。这种自噬激活依赖于细胞外信号调节激酶(ERK)信号通路。使用 ERK 信号通路抑制剂 U0126 可显著下调神经元自噬水平。综上所述,这些结果表明 MH 可以通过 ERK 信号通路适度激活神经元自噬,减少神经细胞死亡,产生神经保护作用。

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