Carvacrol protects against spinal cord injury in rats via suppressing oxidative stress and the endothelial nitric oxide synthase pathway.

Carvacrol (CAR) is a naturally occurring phenolic monoterpene and has been demonstrated to possess a spectrum of pharmacological actions. The present study was designed to assess the neuroprotection of CAR against spinal cord injury (SCI) in rats and to identify the underlying mechanisms. SCI was induced using the modified weight‑drop method in Wistar rats. CAR or saline was administered at doses of 25, 50 and 100 mg/kg for 46 days. Neuronal function following SCI was evaluated using the Basso, Beattie and Bresnahan (BBB) locomotor rating scale. Spinal cord edema was assessed by measuring the water content in spinal cord tissues. The oxidative indicators, including malondialdehyde, catalase, superoxide dismutase glutathione peroxidase and 8‑isoprotane as well as endothelial nitric oxide synthase (eNOS) activity and caspase‑3 were measured using corresponding commercial kits. The protein expression of eNOS and B cell lymphoma‑2 (Bcl‑2) as well as Bcl‑2‑associated X protein (Bax) was analyzed by western blot analysis. The SCI‑induced rats demonstrated marked reductions in BBB scores. CAR treatment recovered neurological function with decreasing BBB scores. CAR was found to have inhibitory effects on the water content in the spinal cord, oxidative stress, eNOS, nitric oxide production and apoptosis‑associated molecules, including Bax and caspase‑3 as well as promoting Bcl-2 expression in SCI-induced rats. These results suggested that CAR protects against SCI via mediating oxidative stress and the eNOS signaling pathway.