Analgesic mechanism of cinobufagin in rats with bone cancer pain / 中草药

ABSTRACT

Objective: To investigate the analgesic mechanism of cinobufagin in rats with bone cancer pain. Methods: Female SD rats meeting the conditions of pain threshold were selected to construct cancer-induced bone pain (CIBP) model. On the 7th day after modeling, the sham group and the model group were administrated by saline, while the treatment groups were administrated with the low, medium and high concentrations of cinobufagin for consecutive 7 d. The pain behavior (mechanical withdrawal threshold and thermal pain threshold) was tested before modeling and after modeling, and single injection of cinobufagin after 0.5, 1, 2, 4, 6, 8 and 24 h at the first day. The expression of MAPKs protein was detected by Western Blotting, and the content of spinal cytokines (IL-1β, TNF-α, MCP-1) was detected by ELISA. Results: The mechanical pain threshold and thermal pain threshold were significantly decreased in the model group, compared with the sham group (P 0.05). Protein levels of MAPKs were increased in the model group, while the levels of JNK and p38 were decreased in the cinobufagin group (P 0.05). ELISA results showed that cinobufagin significantly decreased the content of cytokines in the spinal cord, when compared with the model group (P < 0.05). Conclusion: Cinobufagin can inhibit the expression of MAPKs proteins in the spinal cord of the rat model with bone cancer pain, ultimately decrease the content of IL-1β, TNF-α, and MCP-1 to alleviate the pain during the process of cancer pain.