Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Spine (Phila Pa 1976). 2012 Oct 1;37(21):1810-8. doi: 10.1097/BRS.0b013e31824ffac6.
STUDY DESIGN: Animal model of intravertebral disc (IVD) degeneration. OBJECTIVE: To examine production of inflammatory mediators in IVDs and neuropeptides in dorsal root ganglia (DRGs) in rat models of IVD compression and injury. SUMMARY OF BACKGROUND DATA: Sensory nerve fibers in IVDs and inflammatory mediator responses have been verified in animal models of IVD injury. However, the IVD injury in animals incompletely models degenerated human IVDs causing discogenic low back pain, because human IVDs are also subject to compression. METHODS: Experimental groups (controls, IVD injury, IVD compression, and their combination) of Sprague Dawley rats were prepared. Fluoro-Gold (FG; Fluorochrome, Denver, CO) was applied into coccygeal IVDs. Inflammatory mediators in IVDs, including nerve growth factor, tumor necrosis factor α, interleukin 1β, and interleukin 6, were quantified using enzyme-linked immunosorbent assays. DRGs were immunostained for calcitonin gene-related peptide, activating transcription factor 3, and growth-associated phosphoprotein 43. RESULTS: The upregulation of inflammatory mediators was transient in the IVD injury group but delayed and long-lasting in the IVD compression group. When the IVD injury and compression were combined, the upregulation of inflammatory mediators was long-lasting through 8 weeks. The proportion of calcitonin gene-related peptide-immunoreactive neurons among Fluoro-Gold-labeled neurons remained significantly higher in the IVD injury, compression, and combination groups than in the controls. In contrast, increases in the proportions of activating transcription factor 3-immunoreactive or growth-associated phosphoprotein 43-immunoreactive neurons in the IVD injury group animals were transient but long-lasting in the compression and combination groups compared with controls. CONCLUSION: Disc injury in rats produces persistent increases in neuropeptides in DRGs but only transient increases in inflammatory mediators in IVDs. On the contrary, disc compression in rats produces a long-lasting increase in inflammatory mediators in IVDs and neuropeptides in DRGs. Moreover, disc compression induces persistent nerve injury and regeneration of the afferent fibers innervating IVDs.
研究设计：椎间盘（IVD）退变的动物模型。 目的：在椎间盘压迫和损伤大鼠模型中，检测 IVD 中炎症介质和背根神经节（DRG）中神经肽的产生。 背景资料概要：在椎间盘损伤的动物模型中，已证实感觉神经纤维和炎症介质反应的存在。然而，动物的椎间盘损伤不完全模拟了导致椎间盘源性下腰痛的退变人类椎间盘，因为人类椎间盘也受到压迫。 方法：制备 Sprague Dawley 大鼠的实验组（对照组、椎间盘损伤、椎间盘压迫和它们的组合）。将荧光金（FG；Fluorochrome，丹佛，CO）应用于尾骨椎间盘。使用酶联免疫吸附试验定量 IVD 中的炎症介质，包括神经生长因子、肿瘤坏死因子 α、白细胞介素 1β 和白细胞介素 6。用降钙素基因相关肽、激活转录因子 3 和生长相关磷蛋白 43 对 DRG 进行免疫染色。 结果：椎间盘损伤组的炎症介质上调是短暂的，但椎间盘压迫组是延迟和持久的。当椎间盘损伤和压迫相结合时，炎症介质的上调是持久的，持续 8 周。在椎间盘损伤、压迫和联合组中，荧光金标记神经元中降钙素基因相关肽免疫反应性神经元的比例明显高于对照组。相比之下，在椎间盘损伤组动物中，激活转录因子 3 免疫反应性或生长相关磷蛋白 43 免疫反应性神经元的比例增加是短暂的，但在压迫和联合组中是持久的，与对照组相比。 结论：大鼠椎间盘损伤会导致 DRG 中神经肽持续增加，但 IVD 中炎症介质仅短暂增加。相反，大鼠椎间盘压迫会导致 IVD 中炎症介质和 DRG 中神经肽持续增加。此外，椎间盘压迫会导致支配椎间盘的传入纤维持续神经损伤和再生。
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