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地塞米松对急性脊髓损伤中自噬和凋亡的影响。

Effects of dexamethasone on autophagy and apoptosis in acute spinal cord injury.

作者信息

Wang ZhenYu, Zhou LinQuan, Zheng XiaoTing, Liu WenGe

机构信息

Department of Orthopedics, Affiliated Union Hospital of Fujian Medical University.

Fujian Medical University, Fuzhou.

出版信息

Neuroreport. 2018 Sep 5;29(13):1084-1091. doi: 10.1097/WNR.0000000000001076.

Abstract

Previous studies have indicated that spinal cord injury can induce autophagy. To a certain extent, increased autophagy has a protective effect on neurons. Early hormone therapy is well recognized as a treatment for spinal cord injury. However, whether the protective effect of autophagy is important in recovery from spinal cord injury remains unclear. In this study, we established an in-vitro model of spinal cord injury to study the effects of dexamethasone on mechanical injury, autophagy, and apoptosis in spinal cord neurons. The results showed that dexamethasone inhibited the level of autophagy in the injured nerve cells in a dose-dependent manner. High doses of dexamethasone protected the damaged spinal cord neurons by inhibiting apoptosis, but a protective effect from low hormone concentrations was not obvious. When autophagy was inhibited in damaged spinal cord neurons, apoptosis decreased significantly; in contrast, impairment of autophagy-induced activation of spinal cord neurons and apoptosis levels were significantly increased.

摘要

先前的研究表明,脊髓损伤可诱导自噬。在一定程度上,自噬增加对神经元具有保护作用。早期激素治疗是脊髓损伤公认的一种治疗方法。然而,自噬的保护作用在脊髓损伤恢复中是否重要仍不清楚。在本研究中,我们建立了脊髓损伤体外模型,以研究地塞米松对脊髓神经元机械损伤、自噬和凋亡的影响。结果表明,地塞米松以剂量依赖性方式抑制受损神经细胞中的自噬水平。高剂量地塞米松通过抑制凋亡保护受损的脊髓神经元,但低激素浓度的保护作用不明显。当受损脊髓神经元中的自噬被抑制时,凋亡显著减少;相反,自噬受损诱导脊髓神经元激活且凋亡水平显著增加。

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