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首页> 外文期刊>Journal of orthopaedic research >Interleukin-6 and interleukin-6 receptor expression, localization, and involvement in pain-sensing neuron activation in a mouse intervertebral disc injury model
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Interleukin-6 and interleukin-6 receptor expression, localization, and involvement in pain-sensing neuron activation in a mouse intervertebral disc injury model

机译：小鼠椎间盘损伤模型中白细胞介素6和白细胞介素6受体的表达，定位及其在痛觉神经元激活中的作用

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摘要

The pathological mechanism of intractable low back pain is unclear. However, intervertebral disc (IVD) degeneration is a primary cause of low back pain, and pain-related mediators, such as interleukin-6 (IL-6), have been correlated with discogenic pain. The objective of this study is to elucidate the mechanism of local IL-6 and IL-6 receptor (IL-6R) expression after IVD injury as well as determine the involvement of IL-6/IL-6 signaling in discogenic pain. To do this, quantitative and immunohistological analyses in a mouse model of IVD injury were performed. Firstly, we measured the local expression levels of IL-6 and IL-6R in IVDs by enzyme-linked immunosorbent assay (ELISA). Secondly, we immunohistochemically confirmed their localization in injured IVDs. Lastly, we evaluated the effects of intradiscal injection of an IL-6 inhibitor by evaluating pain-related protein, calcitonin gene-related peptide (CGRP), expression in dorsal root ganglia (DRG) neurons that innervate IVDs. Injured IVDs showed increased production of IL-6 and IL-6R. IL-6 and IL-6R expression in the injured IVD were predominantly localized in the annulus fibrosus and endplate, and intradiscal injection of the IL-6 inhibitor suppressed CGRP expression in the DRG neurons. These results show that IL-6 and IL-6R expression levels are responsive to IVD injury and that inhibition of IL-6/IL-6R signaling may be a promising analgesic treatment for degenerative disc diseases. (c) 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1508-1514, 2015.
机译：顽固性下腰痛的病理机制尚不清楚。然而，椎间盘（IVD）变性是下腰痛的主要原因，并且与疼痛相关的介质，例如白介素6（IL-6），已与椎间盘源性疼痛相关。这项研究的目的是阐明IVD损伤后局部IL-6和IL-6受体（IL-6R）表达的机制，以及确定IL-6 / IL-6信号传导与椎间盘源性疼痛有关。为此，在IVD损伤的小鼠模型中进行了定量和免疫组织学分析。首先，我们通过酶联免疫吸附试验（ELISA）测量了IVDs中IL-6和IL-6R的局部表达水平。其次，我们免疫组化证实了它们在受损IVD中的定位。最后，我们通过评估疼痛相关蛋白，降钙素基因相关肽（CGRP），支配IVD的背根神经节（DRG）神经元的表达，评估了椎间盘内注射IL-6抑制剂的效果。受伤的IVD显示IL-6和IL-6R的产生增加。受损IVD中的IL-6和IL-6R表达主要定位在纤维环和终板中，并且在椎间盘内注射IL-6抑制剂可抑制DRG神经元中的CGRP表达。这些结果表明IL-6和IL-6R表达水平对IVD损伤有反应，并且抑制IL-6 / IL-6R信号传导可能是退行性椎间盘疾病的有希望的止痛药。 （c）2015骨科研究学会。由Wiley Periodicals，Inc.出版，J Orthop Res 33：1508-1514，2015。

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