自噬
脊髓
脊髓损伤
细胞凋亡
地塞米松
医学
程序性细胞死亡
麻醉
内分泌学
生物
生物化学
精神科
作者
Zhen-Yu Wang,Linquan Zhou,Xiaoting Zheng,Wenge Liu
出处
期刊:Neuroreport
[Lippincott Williams & Wilkins]
日期:2018-07-07
卷期号:29 (13): 1084-1091
被引量:18
标识
DOI:10.1097/wnr.0000000000001076
摘要
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.
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