ABSTRACT
Inflammatory pain is known to severely impact the life quality of patients. Notably, dezocine is widely used for the treatment of pain. Therefore, the current study aimed to examine the effects of dezocine on a complete Freund's adjuvant (CFA)-induced inflammatory pain model in rats and to investigate the possible underlying molecular mechanisms. Rats were randomly divided into three groups, including the control, CFA and dezocine+CFA groups, and then subcutaneously injected with 100 µl saline, subcutaneously injected with 100 µl CFA or pretreated with 1 ml dezocine (0.4 µg/kg) at 30 min before CFA injection in the plantar surface of right hind paw, respectively. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were measured with a dynamic plantar esthesiometer at 1 day before and 6 h after CFA injection. The ipsilateral lumbar spinal cords of all the rats were harvested for detecting the expression profiles of phosphorylated (p)-p65, p-extracellular signal-regulated kinase 1/2 (p-ERK1/2), cyclooxygenase-2 (COX-2), interleukin (IL)-1ß and tumor necrosis factor (TNF)-α by western blot analysis and/or reverse transcription-quantitative polymerase chain reaction. In addition, prostaglandin E2 (PGE2) expression was determined by enzyme-linked immunosorbent assay. Compared with the control group, CFA-induced peripheral inflammation downregulated the PWT and PWL values of rats, which were significantly alleviated by dezocine treatment. Furthermore, the protein levels of p-p65, p-ERK1/2, COX-2, PGE2, IL-1ß and TNF-α were significantly upregulated following CFA injection, while they were suppressed by dezocine pretreatment. In conclusion, the analgesic effect of dezocine on inflammatory pain induced by CFA may be associated with the inhibition of the spinal ERK1/2-COX-2 pathway.