Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats
Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats
复制标题
脊髓电压依赖性阴离子通道 1 的上调导致大鼠骨癌疼痛过敏
DOI：
10.1007/s12264-017-0195-1
复制
发表时间：
2017-12-01
影响因子：
5.6
通讯作者：
Jiang, Guo-Qin
中科院分区：
文献类型：
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作者：
Kong, Xiangpeng;Wei, Jinrong;Jiang, Guo-Qin
电压依赖性阴离子通道1(VDAC1)被认为与肿瘤的发展有关。然而，VDAC1是否与骨癌疼痛有关仍不清楚。在本研究中，我们发现在胫骨腔内注射肿瘤细胞后2周和3周，VDAC1在脊髓背角的L2-5节段表达上调。鞘内注射VDAC1抑制剂可显著逆转痛敏反应，减少Toll样受体4(TLR4)的过度表达。鞘内注射米诺环素，一种小胶质细胞的抑制剂，也减轻了骨癌疼痛大鼠模型的疼痛过敏。这些结果提示，VDAC1可能通过调节TLR4的表达，在复杂癌痛的发生发展过程中发挥重要作用。
Voltage-dependent anion channel 1 (VDAC1) is thought to contribute to the progression of tumor development. However, whether VDAC1 contributes to bone cancer pain remains unknown. In this study, we found that the expression of VDAC1 was upregulated in the L2–5 segments of the spinal dorsal horn at 2 and 3 weeks after injection of tumor cells into the tibial cavity. Intrathecal injection of a VDAC1 inhibitor significantly reversed the pain hypersensitivity and reduced the over-expression of Toll-like receptor 4 (TLR4). Intrathecal injection of minocycline, an inhibitor of microglia, also attenuated the pain hypersensitivity of rat models of bone cancer pain. These results suggest that VDAC1 plays a significant role in the development of complicated cancer pain, possibly by regulating the expression of TLR4.