炎症
脊髓损伤
氧化应激
脊髓
体内
化学
超氧化物歧化酶
药理学
细胞生物学
生物
免疫学
生物化学
神经科学
生物技术
作者
Daoyong Li,He Tian,Xian Li,Liang Mao,Xiaojun Zhao,Jiaquan Lin,Sen Lin,Chang Xu,Yuanye Liu,Yuanqiang Guo,Xifan Mei
出处
期刊:Life Sciences
[Elsevier]
日期:2020-03-01
卷期号:245: 117351-117351
被引量:49
标识
DOI:10.1016/j.lfs.2020.117351
摘要
To study the specific therapeutic effect of zinc on spinal cord injury (SCI) and its specific protective mechanism.The effects of zinc ions on neuronal cells were examined in a mouse SCI model and in vitro. In vivo, neurological function was assessed by Basso Mouse Scaleat (BMS) at 1, 3, 5, 7, 10, 14, 21, and 28 days after spinal cord injury. The number of neurons and histomorphology were observed by nissl staining and hematoxylin-eosin staining (HE). The chromatin and mitochondrial structure of neurons were detected by transmission electron microscopy (TEM). The expression of nuclear factor erythroid 2 related factor 2 (Nrf2)-related antioxidant protein and NLRP3 inflammation-related protein were detected in vivo and in vitro by western blot (WB) and immunofluorescence (IF), respectively.Zinc treatment promoted motor function recovery on days 3, 5, 7, 14, 21 and 28 after SCI. In addition, zinc reduces the mitochondrial void rate in spinal neuronal cells and promotes neuronal recovery. At the same time, zinc reduced the levels of reactive oxygen species (ROS) and malondialdehyde in spinal cord tissue after SCI, while increasing superoxide dismutase activity and glutathione peroxidase production. Zinc treatment resulted in up-regulation of Nrf2/Ho-1 levels and down-regulation of nlrp3 inflammation-associated protein expression in vitro and in vivo.Zinc has a protective effect on spinal cord injury by inhibiting oxidative damage and nlrp3 inflammation. Potential mechanisms may include activation of the Nrf 2/Ho-1 pathway to inhibit nlrp3 inflammation following spinal cord injury. Zinc has the potential to treat SCI.
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