Abstract
Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.
Highlights
Spinal cord injury (SCI) is a critical central nervous system disease that can cause permanent damage to nerve function, which is considered to be the main cause of paralysis [1]
We explored the regulatory effects of zinc on the glucose metabolism of the neurons and spinal cord after SCI from two aspects of glucose uptake and mitochondrial protection, and clarified the role of AMPK in it, providing a new idea for the treatment of SCI
In order to explore the protective effect of zinc on PC12 cells, cells were first processed by H2O2
Summary
Spinal cord injury (SCI) is a critical central nervous system disease that can cause permanent damage to nerve function, which is considered to be the main cause of paralysis [1]. SCI is divided into primary injury and secondary injury. Primary injury caused by trauma leads to a series of complex secondary injuries, including oxidative stress, neuronal apoptosis, inflammation, mitochondrial dysfunction, and metabolic disorders [3, 4]. Neurons are sensitive to changes in energy after SCI. Insufficient energy supply caused by impaired ATP synthesis seriously affects the survival of the neurons [5]. Metabolism changes are closely related to the survival of the neurons, but there are currently few studies on the spinal cord and neuronal metabolism after SCI, especially glucose metabolism, which is a problem worthy of attention
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
