Zinc promotes autophagy and inhibits apoptosis through AMPK/mTOR signaling pathway after spinal cord injury
Zinc promotes autophagy and inhibits apoptosis through AMPK/mTOR signaling pathway after spinal cord injury
复制标题
锌通过AMPK/mTOR信号通路促进脊髓损伤后自噬并抑制细胞凋亡
DOI：
10.1016/j.neulet.2020.135263
复制
发表时间：
2020-09-25
影响因子：
2.5
通讯作者：
Mei, Xifan
中科院分区：
文献类型：
--
作者：
Lin, Sen;Tian, He;Mei, Xifan
自噬是一种细胞内生物过程，控制营养剥夺和饥饿的稳态，并与创伤性疾病的发生有关。锌是参与生命活动的重要化学元素，通过腹腔注射具有改善神经恢复的作用。本研究旨在探讨锌对损伤脊髓和神经元自噬和细胞凋亡的调节作用。结果表明，锌通过激活腺苷5′-单磷酸腺苷（AMP）活化蛋白激酶（AMPK）信号通路显著诱导Beclinl和LC3B水平。此外，锌还能抑制损伤脊髓的细胞凋亡。综上所述，这些发现提示锌通过促进神经元自噬和抑制细胞凋亡。
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 Beclinl 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.