Departments of *Bioengineering and †Neurosurgery, University of Pennsylvania, Philadelphia, PA.
Spine (Phila Pa 1976). 2014 Feb 1;39(3):207-12. doi: 10.1097/BRS.0000000000000107.
This study used immunohistochemistry and an enzyme immunoassay to quantify interleukin-1α (IL-1α) and prostaglandin E2 (PGE2) levels in the spinal cord of rats at 1 day after painful cervical facet joint injury.
The objective of this study was to determine to what extent spinal inflammation is initiated early after a painful loading-induced injury of the C6-C7 facet joint in a rat model.
A common source of neck pain, the cervical facet joint is susceptible to loading-induced injury, which can lead to persistent pain. IL-1α and PGE2 are associated with joint inflammation and pain, both locally in the joint and centrally in the spinal cord. Joint inflammation has been shown to contribute to pain after facet joint injury. Although spinal neuronal hyperactivity is evident within 1 day of painful facet injury, it is unknown if inflammatory mediators, such as IL-1α and PGE2, are also induced early after painful injury.
Rats underwent either a painful C6-C7 facet joint distraction or sham procedure. Mechanical sensitivity was assessed, and immunohistochemical and enzyme immunoassay techniques were used to quantify IL-1α and PGE2 expression in the spinal cord at day 1.
Both IL-1α and PGE2 were significantly elevated (P≤ 0.04) at day 1 after painful injury. Moreover, although both spinal IL-1α and PGE2 levels were correlated with the withdrawal threshold in response to mechanical stimulation of the forepaw, this correlation was only significant (P = 0.01) for PGE2.
The increased expression of 2 inflammatory markers in the spinal cord at 1 day after painful joint injury suggests that spinal inflammation may contribute to the initiation of pain after cervical facet joint injury. Further studies will help identify functional roles of both spinal IL-1α and PGE2 in loading-induced joint pain.
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本研究采用免疫组织化学和酶免疫测定法，在大鼠颈关节突关节损伤后 1 天，定量检测脊髓中白细胞介素-1α（IL-1α）和前列腺素 E2（PGE2）的水平。
本研究旨在确定在大鼠模型中，C6-C7 关节突关节受到疼痛性负荷诱导损伤后，早期脊髓炎症的起始程度。
颈部疼痛的常见原因是颈椎关节突关节，易受到负荷诱导损伤，从而导致持续性疼痛。IL-1α 和 PGE2 与关节炎症和疼痛有关，既与关节局部有关，也与脊髓中枢有关。关节炎症已被证明是关节突关节损伤后疼痛的原因之一。尽管在疼痛性关节突损伤后 1 天内明显出现脊髓神经元过度活跃，但尚不清楚炎症介质（如 IL-1α 和 PGE2）是否也在疼痛性损伤后早期诱导。
大鼠行 C6-C7 关节突关节牵拉或假手术。评估机械敏感性，并采用免疫组织化学和酶免疫测定技术，在第 1 天定量检测脊髓中 IL-1α 和 PGE2 的表达。
在疼痛性损伤后第 1 天，IL-1α 和 PGE2 均显著升高（P≤0.04）。此外，尽管脊髓 IL-1α 和 PGE2 水平与前爪机械刺激的退缩阈值均相关，但这种相关性仅对 PGE2 有统计学意义（P=0.01）。
在疼痛性关节突关节损伤后第 1 天，脊髓中 2 种炎症标志物表达增加，表明脊髓炎症可能导致颈椎关节突关节损伤后疼痛的发生。进一步的研究将有助于确定脊髓 IL-1α 和 PGE2 在负荷诱导性关节疼痛中的功能作用。
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