在大鼠疼痛性颈椎小关节损伤后，前列腺素 E2 受体 EP2 在背根神经节中上调。
The prostaglandin E2 receptor, EP2, is upregulated in the dorsal root ganglion after painful cervical facet joint injury in the rat.
机构信息
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
出版信息
Spine (Phila Pa 1976). 2013 Feb 1;38(3):217-22. doi: 10.1097/BRS.0b013e3182685ba1.
STUDY DESIGN
This study implemented immunohistochemistry to assay prostaglandin E2 (PGE2) receptor EP2 expression in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.
OBJECTIVE
To identify if inflammatory cascades are induced in association with cervical facet joint distraction-induced pain by investigating the time course of EP2 expression in the DRG.
SUMMARY OF BACKGROUND DATA
The cervical facet joint is a common source of neck pain, and nonphysiological stretch of the facet capsular ligament can initiate pain from the facet joint via mechanical injury. PGE2 levels are elevated in painful inflamed and arthritic joints, and PGE2 sensitizes joint afferents to mechanical stimulation. Although in vitro studies suggest that the EP2 receptor subtype contributes to painful joint disease, the EP2 response has not been investigated for any association with painful mechanical joint injury.
METHODS
Separate groups of male Holtzman rats underwent either a painful cervical facet joint distraction injury or sham procedure. Bilateral forepaw mechanical allodynia was assessed, and immunohistochemical techniques were used to quantify EP2 expression in the DRG at days 1 and 7.
RESULTS
Facet joint distraction induced mechanical allodynia that was significant (P < 0.024) at all time points. Painful joint injury also significantly elevated total EP2 expression in the DRG at day 1 (P = 0.009), which was maintained at day 7 (P < 0.001). Neuronal expression of EP2 in the DRG was only increased over sham levels at day 1 (P = 0.013).
CONCLUSION
Painful cervical facet joint distraction induces an immediate and sustained increase of EP2 expression in the DRG, implicating peripheral inflammation in the initiation and maintenance of facet joint pain. The transient increase in neuronal EP2 suggests, as in other painful joint conditions, that after joint injury nonneuronal cells may migrate to the DRG, some of which likely express EP2.
研究设计
本研究通过免疫组织化学方法检测疼痛性颈椎小关节损伤后大鼠背根神经节（DRG）中前列腺素 E2（PGE2）受体 EP2 的表达。
目的
通过研究 DRG 中 EP2 表达的时间过程，确定颈椎小关节分离引起的炎症级联反应是否与颈椎小关节疼痛有关。
背景资料概要
颈椎小关节是颈部疼痛的常见来源，小关节囊韧带的非生理伸展可通过机械损伤引发小关节疼痛。疼痛性炎症和关节炎关节中的 PGE2 水平升高，PGE2 使关节传入纤维对机械刺激敏感。尽管体外研究表明 EP2 受体亚型有助于疼痛性关节疾病，但尚未研究 EP2 反应与疼痛性机械关节损伤的任何关联。
方法
分别将雄性霍尔茨曼大鼠进行疼痛性颈椎小关节分离损伤或假手术。评估双侧前爪机械性痛觉过敏，并在 DRG 中使用免疫组织化学技术在第 1 天和第 7 天量化 EP2 表达。
结果
小关节分离引起机械性痛觉过敏，所有时间点均有显著差异（P <0.024）。疼痛性关节损伤也显著增加了 DRG 中 EP2 的总表达，第 1 天（P = 0.009），第 7 天（P <0.001）。DRG 中 EP2 的神经元表达仅在第 1 天（P = 0.013）比假手术水平升高。
结论
疼痛性颈椎小关节分离引起 DRG 中 EP2 表达的即刻和持续增加，提示外周炎症参与了小关节疼痛的发生和维持。神经元 EP2 的短暂增加表明，在其他疼痛性关节疾病中，关节损伤后非神经元细胞可能迁移到 DRG，其中一些可能表达 EP2。
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