Neuroprotective effects of dexmedetomidine in spinal cord injury via modulating PERK/ATF4 pathway.

OBJECTIVES

This study explored whether dexmedetomidine (DEX) can promote functional restoration following spinal cord injury (SCI) through the PKR-like endoplasmic reticulum kinase (PERK)/activating transcription factor 4 (ATF4) pathway.

METHODS

A rat T10 SCI model was established with 5 groups including sham, SCI, PERK agonist, DEX, and DEX + PERK agonist. The protective role of the PERK/ATF4 pathway in DEX was investigated by comparing autophagy, inflammatory cytokines, and neurological function recovery in each group.

RESULTS

Seven days after the surgical procedure, DEX administration facilitated neurological recovery by activating autophagy and restraining inflammatory cytokines through the PERK/ATF4 pathway.

CONCLUSION

The PERK signaling may be associated with DEX-mediated neuroprotection, potentially involving the induction of autophagy and suppression of inflammation.