Objective
Incomplete spinal cord injury (SCI) is the most common spinal cord injury in clinic, however its mechanism is still not fully understood. Design: We constructed the rabbit spinal cord hemisection (SCH) model and used RT-PCR, western blotting, immunohistochemistry, and immunofluorescence experiments to explore the potential mechanism of SCI. Setting: The sham operation (SH) group, the observation (OB, which is the SCH) group, the OB+ substance p (SP) inhibitor group, the OB + NK1R inhibitor group, the OB + NK1R agonist group and the OB + SP inhibitor + NK1R agonist group. Participants: New Zealand white rabbits. Interventions: Use NK1R inhibitors, NK1R agonists, SP inhibitors to treat the SCH model. Outcome measures: IL-1β, IKKγ, IL-6 and NF-κB.
Results
The results showed that nissl bodies, inflammatory cells and SP increased notably in the spinal cord cells of the rabbit SCH model. Through in vivo experiments with SP or NK1R inhibitors or NK1R agonists, we found that inhibiting SP/NK1R signaling can help improve SCH by inhibiting the release of pro-inflammatory cytokines IL-1β, IKKγ, IL-6 and NF-κB. Registered trials: Animal experiments were approved by Ruijin Hospital, Shanghai Jiaotong University School of Medicine.