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目的观察脊髓单核细胞趋化蛋白受体CCR2在大鼠骨癌痛形成过程中的可能机制。方法大鼠左侧胫骨骨髓腔内接种Walker256乳腺癌细胞制备骨癌痛模型。观察并测量各组大鼠术前1 d,术后3、6、9、10、11、12 d的机械痛阈值。术后12 d取材,免疫组织化学法检测脊髓背角星形胶质细胞标志物(GFAP)的平均光密度值(MOD),观察脊髓小胶质细胞增殖活化情况。结果与对照组相比,鞘内给予CCR2拮抗剂后大鼠机械痛阈值明显升高,脊髓GFAP表达明显降低(P<0.01)。结论鞘内注射CCR2特异性拮抗剂可能通过抑制脊髓星形胶质细胞的活化而缓解大鼠骨癌痛,CCR2可能是治疗骨癌痛新的靶点。
Objective To investigate the possible mechanism of spinal cord monocyte chemoattractant protein receptor CCR2 in rat bone cancer pain. Methods Walker256 breast cancer cells were inoculated into the left tibial bone marrow cavity to prepare bone cancer pain model. The mechanical pain thresholds of rats in each group were observed and measured on the 1st day, the 3rd, 6th, 9th, 10th, 11th and 12th day after operation. Twelve days after the operation, the average optical density (MOD) of spinal cord astrocyte marker (GFAP) was detected by immunohistochemistry and the proliferation and activation of spinal cord microglia were observed. Results Compared with the control group, the CCR2 antagonist significantly increased the mechanical threshold and the GFAP expression in the spinal cord (P <0.01). Conclusion Intrathecal injection of CCR2-specific antagonists may relieve bone cancer pain in rats by inhibiting the activation of spinal cord astrocytes. CCR2 may be a new target for the treatment of bone cancer pain.