AIMS To study the specific therapeutic effect of zinc on spinal cord injury (SCI) and its specific protective mechanism. MAIN METHODS 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. KEY FINDINGS 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. SIGNIFICANCE 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.

中文翻译：

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锌可通过激活Nrf2 / HO-1防御途径并抑制神经细胞中NLRP3的炎症来促进脊髓损伤后的功能恢复。

目的研究锌对脊髓损伤（SCI）的特异性治疗作用及其特异性保护机制。主要方法在小鼠SCI模型中和体外检查了锌离子对神经元细胞的影响。在体内，脊髓损伤后第1、3、5、7、10、14、21和28天通过Basso Mouse Scaleat（BMS）评估神经功能。通过nissl染色和苏木精-伊红染色（HE）观察神经元的数目和组织形态。通过透射电子显微镜（TEM）检测神经元的染色质和线粒体结构。通过Western blot（WB）和免疫荧光（IF）分别在体内和体外检测核因子红系2相关因子2（Nrf2）相关的抗氧化剂蛋白和NLRP3炎症相关蛋白的表达。主要发现锌治疗在SCI后第3、5、7、14、21和28天促进了运动功能的恢复。另外，锌降低了脊髓神经元细胞中的线粒体空隙率并促进了神经元的恢复。同时，锌降低了脊髓损伤后脊髓组织中活性氧（ROS）和丙二醛的水平，同时增加了超氧化物歧化酶活性和谷胱甘肽过氧化物酶的产生。锌处理在体外和体内导致Nrf2 / Ho-1水平的上调和与炎症反应相关的nlrp3蛋白表达的下调。重要性锌通过抑制氧化损伤和nlrp3炎症对脊髓损伤具有保护作用。潜在的机制可能包括激活Nrf 2 / Ho-1途径以抑制脊髓损伤后的nlrp3炎症。