Blocking SP/NK1R signaling improves spinal cord hemisection by inhibiting the release of pro-inflammatory cytokines in rabbits

Abstract

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.

Zuogui Wan alleviates ovariectomy-induced osteoporosis by maintaining FoxO3 and increasing NK1R

“…NK1R is expressed by osteoblast osteoclasts and their progenitors (22). SP and other neuropeptides by binding to receptors to control the function of osteoclasts and osteoblasts and participate in bone repair, reconstruction and growth.…”