Zinc deficiency impairs axonal regeneration and functional recovery after spinal cord injury by modulating macrophage polarization via NF-kB pathway

Spinal cord injury (SCI) often leads to permanent paralysis, and there's a need for effective treatments. This study explores zinc's role, an essential trace element, in managing inflammatory responses after SCI. The research examines how different levels of zinc in the diet affect the inflammation, nerve regeneration, and overall recovery in mice with spinal cord injuries. The study suggests that ensuring sufficient zinc levels, possibly through supplementation, could be a new way to support recovery after spinal cord injuries.

• 1
  Zinc deficiency after SCI promotes the translocation of NF-kB in macrophages, leading to a pro-inflammatory phenotype and increased expression of pro-inflammatory cytokines.
• 2
  The inflammatory response worsened by zinc deficiency resulted in poorer motor function due to increased apoptosis of oligodendrocytes, demyelination, and inhibited axonal regeneration.
• 3
  Zinc supplementation attenuated these zinc-deficiency-induced responses and improved motor function, indicating its potential as a therapeutic strategy for SCI.