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Zinc promotes autophagy and inhibits apoptosis through AMPK/mTOR signaling pathway after spinal cord injury.
Neuroscience Letters ( IF 2.5 ) Pub Date : 2020-07-16 , DOI: 10.1016/j.neulet.2020.135263
Sen Lin 1 , He Tian 2 , Jiaquan Lin 1 , Chang Xu 1 , Yajiang Yuan 1 , Shuang Gao 1 , Changwei Song 1 , Pengfei Lv 2 , Xifan Mei 1
Affiliation  

Autophagy is a intracellular biological process that controls the homeostasis of nutrition deprivation and starvation and has been associated with the development of traumatic diseases. Zinc, an important chemical element involved in life activities, has improved nerve recovery effects through intraperitoneal injection. The purpose of this study was to probe the possible modulation of autophagy and apoptosis from the injured spinal cord and neurons by zinc administration. It was shown that zinc significantly induced the level of Beclin1 and LC3B by activating adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway. In addition, zinc suppressed apoptosis in the injured spinal cord. Taken together, these findings suggested that zinc through promoting neurons autophagy and inhibiting apoptosis.



中文翻译:

锌在脊髓损伤后通过AMPK / mTOR信号通路促进自噬并抑制细胞凋亡。

自噬是一种细胞内生物学过程,可控制营养缺乏和饥饿的体内平衡,并与创伤性疾病的发展有关。锌是生命活动中的重要化学元素,通过腹膜内注射改善了神经的恢复作用。这项研究的目的是探讨锌给药对受损脊髓和神经元自噬和凋亡的可能调节作用。结果表明,锌通过激活5'-单磷酸腺苷(AMP)激活的蛋白激酶(AMPK)信号传导途径,显着诱导Beclin1和LC3B的水平。此外,锌抑制了受损脊髓的凋亡。综上所述,这些发现表明锌通过促进神经元自噬和抑制细胞凋亡。

更新日期:2020-07-22
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