Department of Orthopaedic Surgery, Tokyo Women's Medical University, Tokyo, Japan.
Spine (Phila Pa 1976). 2011 May 20;36(12):926-32. doi: 10.1097/BRS.0b013e3181e7f4a9.
The mechanisms of apoptosis behind the formation of tissue reactions at the surface of the dorsal root ganglion (DRG) exposed to the nucleus pulposus were studied with special reference to the role of interleukin-6 (IL-6), using electron microscopy and immunohistochemistry in rats.
To study the role of IL-6 on the DRG.
It has been reported that nucleus pulposus cells are capable to produce proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and IL-6. Recently, it was observed that local application of nucleus pulposus induced a characteristic tissue reaction at the surface of the DRG. This change was due to apoptosis of DRG neurons. However, the role of IL-6 is not known regarding the apoptosis of the DRG neurons.
Recombinant IL-6 was applied between the L4 DRG and the dura to mimic a disc herniation of the L4-L5 disc in rats. The L4 DRGs were resected 24 hours after surgery. The sections were processed for immunohistochemistry using antisera to TNF-α. Furthermore, the sections of the specimens were observed using light and electron microscopy to confirm the induced apoptosis of the DRG neurons. The sections were also processed for immunohistochemistry, using antisera to single-stranded DNA (ssDNA) and Caspase 3.
TNF-α immunoreactivity was observed in the peripheral area of DRG at the site of the application of IL-6. Typical changes of the cell nuclei were observed in the DRG by light and electron microscopy, indicating the presence of apoptosis. The presence of ssDNA and Caspase 3 further enhanced the impression that there was apoptosis of the DRG neurons.
IL-6 seemed to induce TNF-α at the surface of DRG exposed to IL-6 and to induce a characteristic reaction at the surface of the DRG. IL-6 may thus play an important role in nucleus pulposus-induced apoptosis of the DRG neurons as well as TNF-α.
本研究通过电子显微镜和免疫组织化学方法，特别关注白细胞介素 6（IL-6）的作用，研究了背根神经节（DRG）表面组织反应形成过程中的细胞凋亡机制，该反应与暴露于髓核的 DRG 有关。
研究 IL-6 在 DRG 中的作用。
已有报道称，髓核细胞能够产生促炎细胞因子，包括肿瘤坏死因子-α（TNF-α）和 IL-6。最近，人们观察到局部应用髓核会在 DRG 表面引起特征性的组织反应。这种变化是由于 DRG 神经元凋亡引起的。然而，关于 DRG 神经元凋亡，IL-6 的作用尚不清楚。
在大鼠的 L4 DRG 和硬脑膜之间应用重组 IL-6，以模拟 L4-L5 椎间盘的椎间盘突出。手术后 24 小时切除 L4 DRG。使用抗 TNF-α 血清对标本进行免疫组织化学处理，对切片进行处理。此外，使用抗单链 DNA（ssDNA）和 Caspase 3 的抗血清对标本的切片进行观察，以确认 DRG 神经元的诱导性凋亡。
在应用 IL-6 的 DRG 外周区域观察到 TNF-α 免疫反应性。通过光镜和电镜观察到 DRG 细胞核的典型变化，表明存在细胞凋亡。ssDNA 和 Caspase 3 的存在进一步增强了 DRG 神经元发生凋亡的印象。
IL-6 似乎在暴露于 IL-6 的 DRG 表面诱导 TNF-α，并在 DRG 表面诱导特征性反应。因此，IL-6 可能在髓核诱导的 DRG 神经元凋亡以及 TNF-α中发挥重要作用。
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