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2
The Mitochondrial Voltage-Dependent Anion Channel 1, Ca Transport, Apoptosis, and Their Regulation.线粒体电压依赖性阴离子通道1、钙转运、细胞凋亡及其调控
Front Oncol. 2017 Apr 10;7:60. doi: 10.3389/fonc.2017.00060. eCollection 2017.
3
Overexpression of suppressor of cytokine signaling 3 in dorsal root ganglion attenuates cancer-induced pain in rats.背根神经节中细胞因子信号传导抑制因子3的过表达减轻大鼠癌症诱导的疼痛。
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Diclofenac pretreatment modulates exercise-induced inflammation in skeletal muscle of rats through the TLR4/NF-κB pathway.双氯芬酸预处理通过TLR4/NF-κB途径调节大鼠骨骼肌运动诱导的炎症。
Appl Physiol Nutr Metab. 2017 Jul;42(7):757-764. doi: 10.1139/apnm-2016-0593. Epub 2017 Feb 24.
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Down-Regulation of CXCL12/CXCR4 Expression Alleviates Ischemia-Reperfusion-Induced Inflammatory Pain via Inhibiting Glial TLR4 Activation in the Spinal Cord.CXCL12/CXCR4表达下调通过抑制脊髓胶质细胞TLR4激活减轻缺血再灌注诱导的炎性疼痛。
PLoS One. 2016 Oct 19;11(10):e0163807. doi: 10.1371/journal.pone.0163807. eCollection 2016.
6
Modulation of Nav1.8 by Lysophosphatidic Acid in the Induction of Bone Cancer Pain.溶血磷脂酸对Nav1.8的调节在骨癌疼痛诱导中的作用
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The cystine/glutamate antiporter system xc- drives breast tumor cell glutamate release and cancer-induced bone pain.胱氨酸/谷氨酸逆向转运体系统xc-驱动乳腺肿瘤细胞释放谷氨酸并引发癌症诱导的骨痛。
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Effects of Src-kinase inhibition in cancer-induced bone pain.Src激酶抑制对癌症诱导的骨痛的影响。
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Differences in electrophysiological properties of functionally identified nociceptive sensory neurons in an animal model of cancer-induced bone pain.癌症诱导骨痛动物模型中功能鉴定的伤害性感觉神经元电生理特性的差异。
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脊髓电压门控阴离子通道 1 的上调导致大鼠骨癌痛敏。

Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats.

机构信息

Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psychiatric Diseases and Institute of Neuroscience, The Second Affiliated Hospital, Soochow University, Suzhou, 215123, China.

Center for Translational Medicine, Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, 215600, China.

出版信息

Neurosci Bull. 2017 Dec;33(6):711-721. doi: 10.1007/s12264-017-0195-1. Epub 2017 Dec 1.

DOI:10.1007/s12264-017-0195-1
PMID:29196874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5725391/
Abstract

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.

摘要

电压门控阴离子通道 1(VDAC1)被认为有助于肿瘤发展。然而,VDAC1 是否有助于骨癌疼痛尚不清楚。在这项研究中,我们发现肿瘤细胞注入胫骨腔后 2 至 3 周,VDAC1 的表达在 L2-5 脊髓背角节段上调。鞘内注射 VDAC1 抑制剂可显著逆转痛觉过敏,并降低 Toll 样受体 4(TLR4)的过度表达。鞘内注射小胶质细胞抑制剂米诺环素也可减轻骨癌痛大鼠模型的痛觉过敏。这些结果表明,VDAC1 在复杂癌痛的发展中起重要作用,可能通过调节 TLR4 的表达。