Shuangfeng Li1,2, Bishan Ouyang2, Xin Zhao3, Yaping Wang1. 1. Department of Anesthesiology, Second Xiangya Hospital of Central South University, Changsha 410011, China. 2. Department of Anesthesiology, Hainan General Hospital, Haikou 570311, China. 3. Department of Neurology, Third Xiangya Hospital of Central South University, Changsha 410013, China.
Abstract
OBJECTIVE: To investigate the analgesic effect of dexmedetomidine (Dex) on oxaliplatin-induced neuropathic pain in rats and explore its mechanism. METHODS: SD rats were randomly divided into control, model, Dextreatment, and Dex + atipamezole groups. In the latter 3 groups, rat models of neuropathic pain were established by a single intraperitoneal injection of oxaliplatin. The paw withdrawal threshold (PWT) to mechanical stimuli and tail withdrawal latency (TWL) to thermal stimuli of the rats were determined. Western blotting and immunofluorescence assay were performed to observe the expression of spinal phosphorylated STAT3 (p-STAT3) in the rats. RESULTS: Compared with the rats in the control group, the rats in the model group and Dex+atipamezole group showed significantly decreased PWT and TWL (cold) and increased expression of p-STAT3 in the spinal cord (P < 0.05). In Dex group, PWT and TWL (cold) were significantly increased (P < 0.05) and p-STAT3 expression in the spinal cord was significantly decreased (P < 0.01) 60 to 120 after Dex treatment as compared with those in the model group, and these effects of Dex were significantly attenuated by the administration of atipamezole (P < 0.05). CONCLUSIONS: Dex can alleviate oxaliplatin-induced neuropathic pain in rats by inhibiting the phosphorylation of STAT3 in the spinal cord.
OBJECTIVE: To investigate the analgesic effect of dexmedetomidine (Dex) on oxaliplatin-induced neuropathic pain in rats and explore its mechanism. METHODS: SD rats were randomly divided into control, model, Dextreatment, and Dex + atipamezole groups. In the latter 3 groups, rat models of neuropathic pain were established by a single intraperitoneal injection of oxaliplatin. The paw withdrawal threshold (PWT) to mechanical stimuli and tail withdrawal latency (TWL) to thermal stimuli of the rats were determined. Western blotting and immunofluorescence assay were performed to observe the expression of spinal phosphorylated STAT3 (p-STAT3) in the rats. RESULTS: Compared with the rats in the control group, the rats in the model group and Dex+atipamezole group showed significantly decreased PWT and TWL (cold) and increased expression of p-STAT3 in the spinal cord (P < 0.05). In Dex group, PWT and TWL (cold) were significantly increased (P < 0.05) and p-STAT3 expression in the spinal cord was significantly decreased (P < 0.01) 60 to 120 after Dex treatment as compared with those in the model group, and these effects of Dex were significantly attenuated by the administration of atipamezole (P < 0.05). CONCLUSIONS:Dex can alleviate oxaliplatin-induced neuropathic pain in rats by inhibiting the phosphorylation of STAT3 in the spinal cord.