持续动态机械加压诱导腰椎关节突关节源性腰痛大鼠模型的建立和观察

Establishment and observation of a rat model of lumbar facet joint-derived low back pain induced by intraspinal persistent compressive injury

目的:尝试通过棘突间持续动态机械加压,诱导建立腰椎关节突关节源性腰痛大鼠模型,探讨关节突关节源性腰痛的发病机制。方法:通过棘突间置入加压弹簧,在实验组大鼠中构建腰椎关节突关节持续动态加压模型,并与对照组大鼠和空白组大鼠进行对照,从大鼠疼痛相关行为学和关节突关节滑膜TNF-α和IL-1β表达量两方面进行评估。疼痛行为学的评价方法包括von Frey机械刺激缩足反射阈值测量、热缩足反射潜伏期测量、步态分析,从而建立大鼠关节突关节源性腰痛模型。结果:实验组大鼠疼痛相关行为学与对照组和空白组比较,均发生明显改变,包括von Frey机械刺激缩足反射阈值降低、热刺痛阈值降低、足印面积减小、支撑相缩短、摆动相延长、摆动速度降低,同时实验组大鼠关节突关节滑膜TNF-α和IL-1β含量均较对照组和空白组明显升高。结论:通过向大鼠活体内植入棘突间加压弹簧,实现大鼠腰椎关节突关节持续机械动态加压,能够成功构建机械诱导型大鼠腰椎关节突关节源性腰痛动物模型,可为关节突关节源性腰痛的发病机制和治疗研究提供研究思路和素材。

Objective:To study the pathogenesis of lumbar facet joint-derived low back pain,by developing a novel animal model of facet joint related low back pain by intraspinal persistent compressive injury.Methods:Intraspinal compressive springs were implanted into SD rats as experimental group to induce persisting compressive injury to lumbar facet joint.Facet-derived low back pain animal models were measured by detecting pain behaviors(including paw withdrawal threshold,thermal withdrawal latency and gait analysis)and TNF-αand IL-1βlevels in the synovium.Results:Compared with control group and naive group,the painrelated behaviors of the rats in the experimental group changed significantly.The thresholds of mechanical pain and thermal pain were decreased obviously in experimental group.The experimental group rats presented smaller print area,shorter stance phase,longer swing phase,and lower swing speed.The concentrations of TNF-αand IL-1βin experimental group were increased compared with control group.Conclusion:The rat model of lumbar facet joint-derived low back pain was established successfully by implanting a compression spring between the spinous processes to produce the continuous mechanical dynamic compression for the lumbar facet joints,which could provide research ideas and materials for the pathogenesis and treatment of facet joint-derived low back pain.