Neurological research · 2025
Neuroprotective effects of dexmedetomidine in spinal cord injury via modulating PERK/ATF4 pathway.
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Yang Lijun, Long Bo, Yang Huijun
Аннотация
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.
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.