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中文摘要：
目的观察脊髓趋化因子单核细胞趋化蛋白-1（monocyte chemotactic protein-1,MCP-1,或CCL2）在骨癌痛大鼠中的可能作用。方法大鼠胫骨骨髓腔接种Walker256肿瘤细胞建立骨癌痛模型。观测造模前、后大鼠机械性痛觉超敏Von Frey阈值并观察造模后d 10～12,鞘内给予MCP-1中和抗体对大鼠Von Frey阈值和脊髓小胶质细胞激活标志物（ox-42）表达的影响。结果大鼠种瘤后6～12 d,机械性痛觉超敏Von Frey阈值进行性下降（P〈0.01）;与对照组相比,鞘内给予MCP-1中和抗体后,脊髓ox-42的表达水平明显降低（P〈0.01）,Von Frey阈值的明显升高（P〈0.01）。结论大鼠鞘内注射MCP-1中和抗体缓解骨癌痛,其机制可能与抑制小胶质细胞的激活相关。
英文摘要：
Aim To investigate the possible role of monocyte chemotactic protein-1（MCP-1,or CCL2）in spinal cord in rat model of bone cancer pain.Methods The bone cancer pain model was developed by inoculating Walker256 mammary gland carcinoma cells into the tibia medullary cavity.The change of Von-Frey threshold for mechanical allodynia was observed before and after inoculation.MCP-1 neutralizing antibody or control IgG was injected intrathecally（i.t.） during the period from 10th to 12th day.The effect of intrathecal injection of MCP-1 neutralizing antibody on ox-42（microglia marker） expression in spinal dorsal horn and mechanical allodynia was observed.Result From the 6th to 12th day after inoculation,Von-Frey threshold was significantly decreased（P0.01）.Intrathecal MCP-1 neutralizing antibody significantly suppressed the expression of ox-42 in spinal dorsal horn（P0.01） and increased Von-Frey threshold（P0.01）.Conclusion Intrathecal MCP-1 neutralizing antibody reduces mechanical allodynia in rat model of bone cancer pain,it may inhibit the activation of microglia.
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