Thalidomide alleviates bone cancer pain by down-regulating expressions of NF-κB and GFAP in spinal astrocytes in a mouse model

摘要

Aim: Thalidomide is one of the first line therapies in cancer pain management. Previous study has shown that thalidomide decreases the expression of tumor necrosis factor alpha in the mouse spinal cord. However, the exact cellular and molecular mechanism underlying the effect of thalidomide remains unclear. Here, we investigated the effect of thalidomide on the expression level of NF-κB as well as glial fibrillary acidic protein (GFAP) in the spinal cord astrocyte in a mice model. Materials and methods: MC57G fibrosarcoma cells were intramedullary injected into the right femurs of C57/BL mice to induce behaviors related to bone cancer pain. Postoperative thalidomide was administered intraperitoneally to the mice at dose of 100mg/kg/day for 7days. The effect of thalidomide on pain hypersensitivity was checked by behavioral testing. The expression levels of NF-κB and GFAP in spinal cord were evaluated by using Western blotting and Immunohistochemistry. Results: Compared with the controls, the tumor-bearing mice showed substantial pain-related behaviors. Furthermore, the expression levels of both NF-κB and GFAP increased significantly in the spinal cord astrocytes of the tumor-bearing mice. Treating the tumor-bearing mice with thalidomide results in a dramatic reduction in pain behaviors and a significant decrease of NF-κB and GFAP expressions. Conclusions: Thalidomide alleviates the pain behaviors probably by down-regulating the expression of NF-κB and GFAP.