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To investigate the protective effect of dexmedetomidine (Dex) on traumatic spinal cord injury (TSCI) and to evaluate the involvement of inhibition of endoplasmic reticulum (ER) stress response in the potential mechanism. Sprague–Dawley rats were randomly divided into five groups. The hind limb locomotor function of rats was evaluated at 1, 3 and 7 days after the operation. At 7 days after the operation, spinal cord specimens were obtained for hematoxylin and eosin (H&amp;E), Nissl and TUNEL staining, as well as immunofluorescence and Western blot analyses to detect the level of apoptosis and the levels of proteins related to ER stress. 7 days after the operation, Dex treatment promoted the recovery and also inhibited apoptosis of neurons in the spinal cord. Additionally, Dexinhibited the expression of proteins related to ER stress response after spinal cord injury. Dex improves the neurological function of rats with TSCI and reduces apoptosis of spinal cord neurons. The potential mechanism is related to the inhibition of the ER stress response.

Dexmedetomidine alleviates traumatic spinal cord injury in rats via inhibiting apoptosis induced by endoplasmic reticulum stress