MCP-1 Regulates Fractalkine Secretion through p38MAPK Signaling Pathway in Rats with Advanced Bone Cancer Pain

To explore the effect and mechanism of monocyte chemoattractant-1 regulating fractalkine secretion of neurons through p38mitogen-activated protein kinase signaling pathway in rats with advanced bone cancer pain. 30 adult female Sprague-Dawley rats of clean grade were selected and 5 Sprague-Dawley rats were selected as sham group. The rest rats were injected Walker 256 tumor cells to establish rat bone cancer pain model. After successful modeling, some rats were divided into 6 d group, 12 d group and 18 d group at random. The monocyte chemoattractant-1 protein in spinal cord was compared at 0 h, 1 h, 2 h, 4 h and 24 h. The rest of the model rats were randomly divided into bone cancer pain group and monocyte chemoattractant-1 group. The rats in the bone cancer pain group were not treated. The monocyte chemoattractant-1 rats were intrathecally injected with 10 mu g/mu l monocyte chemoattractant-1 neutralizing antibody. After 12 d, the pain threshold PWT, phopho-p38, chemokine C-X3-C-motif receptor 1 protein expression levels and fractalkine secretion were detected in sham group, bone cancer pain group and monocyte chemoattractant-1 group 12 d later. The monocyte chemoattractant-1 protein in spinal cord of 6 d group, 12 d group and 18 d group was higher than sham group. After 12 d, PWT value of bone cancer pain group was lower than sham group. The PWT value of monocyte chemoattractant-1 group was higher than bone cancer pain group. The phopho-p38, chemokine C-X3-C-motif receptor 1 and fractalkine secretion in spinal cord of bone cancer pain group were higher than sham group. The phopho-p38, chemokine C-X3-C-motif receptor 1 and fractalkine secretion in spinal cord of monocyte chemoattractant-1 group were lower than bone cancer pain group. The monocyte chemoattractant-1 is up-regulated in rats with advanced bone cancer pain, which can regulate the secretion of fractalkine by activating p38 mitogen-activated protein kinase signaling pathway, and then act on chemokine C-X3-C-motif receptor 1 and participate in the process of bone cancer pain in rats.