Inhibition of inflammatory cytokines after early decompression may mediate recovery of neurological function in rats with spinal cord injury

Abstract

A variety of inflammatory cytokines are involved in spinal cord injury and influence the recovery of neuronal function. In the present study, we established a rat model of acute spinal cord injury by cerclage. The cerclage suture was released 8 or 72 hours later, to simulate decompression surgery. Neurological function was evaluated behaviorally for 3 weeks after surgery, and tumor necrosis factor α immunoreactivity and apoptosis were quantified in the region of injury. Rats that underwent decompression surgery had significantly weaker immunoreactivity of tumor necrosis factor α and significantly fewer apoptotic cells, and showed faster improvement of locomotor function than animals in which decompression surgery was not performed. Decompression at 8 hours resulted in significantly faster recovery than that at 72 hours. These data indicate that early decompression may improve neurological function after spinal cord injury by inhibiting the expression of tumor necrosis factor α.

Keywords

• Alzheimer′s disease
• amyloid-β
• astrocytes
• Ca 2+
• calcilytic
• calcium-sensing receptor
• nitromemantine
• NPS 2143
• α7-nicotinic acetylcholine receptor
• nerve regeneration
• spinal cord injury
• surgical decompression
• tumor necrosis factor α
• cell apoptosis
• neurological function
• neural regeneration