Reduction of neuronal damage and promotion of locomotor recovery after spinal cord injury by early administration of methylprednisolone: possible involvement of autophagy pathway (Retracted article. See vol. 12, pg. 26565, 2022)

Reduction of neuronal damage and promotion of locomotor recovery after spinal cord injury by early administration of methylprednisolone: possible involvement of autophagy pathway (Retracted article. See vol. 12, pg. 26565, 2022)
复制标题

早期给予甲基强的松龙可减少脊髓损伤后的神经元损伤并促进运动恢复:可能涉及自噬途径

DOI:
10.1039/c6ra25794a
复制
发表时间:
2017-01-01
期刊:
影响因子:
3.9
通讯作者:
Zhang, Xiaohua
Zhang, Xiaohua
中科院分区:
化学3区
文献类型:
--
作者:
Jin, Yichao;Yang, Shaofeng;Zhang, Xiaohua

文献摘要

相似文献

自噬参与了脊髓损伤后的继发性损伤,但其作用机制尚不清楚。目前还没有关于急性SCI后甲基强的松龙(MP)治疗后自噬变化的报道。在本研究中,我们检测了自噬和凋亡的变化,并探讨了自噬和凋亡之间可能的关系。结果发现,钳夹致大鼠脊髓损伤后不同时间点损伤区细胞凋亡,MP治疗可明显减少损伤区细胞凋亡;我们还发现SCI可以诱导损伤区域中自噬的增加,并且神经元和星形胶质细胞都与自噬生物标志物共染色,包括微管相关蛋白轻链-3和Beclin-1,和凋亡生物标志物半胱氨酸天冬氨酸特异性蛋白酶-3; MP治疗也可促进SCI后的运动恢复。结果表明MP处理后自噬的增加可能是通过抑制细胞凋亡的神经保护机制。
Autophagy is involved in the secondary damage associated with spinal cord injury (SCI), however, the role of autophagy remains to be elucidated. There are no reports regarding changes in autophagy after methylprednisolone (MP) treatment after acute SCI. In the present study, we examined changes in autophagy and apoptosis and explored the possible relationship between autophagy and apoptosis. We found that SCI produced by clamp force in rats caused apoptotic cell death in the injured area at different time points and MP treatment could significantly decrease the number of apoptotic cells; we also found that SCI could induce an increase in autophagy in the injured area and both neurons and astrocytes were co-stained with autophagic biomarkers, including microtubule-associated protein light chain-3 and Beclin-1, and an apoptotic biomarker, cysteinyl aspartate specific proteinase-3; MP treatment could also promote the locomotor recovery after SCI. The results suggest an increase in autophagy after MP treatment may be a neuroprotective mechanism via inhibition of apoptosis.