点拨腰大肌干预椎间盘损伤大鼠模型的实验研究

Experimental Study of Plucking Psoas Major Muscles on Intervertebral Disc Injury Rat Model

目的:通过前路针刺损伤椎间盘建立腰椎间盘损伤大鼠模型,观察该模型是否伴有腰大肌被动拉伸张力变化以及点拨腰大肌对模型的影响。方法:将Wistar雄性大鼠随机分为假手术组、模型组与治疗组,通过前路手术损伤椎间盘造模。治疗组行点拨腰大肌干预,隔日1次,共10次。观察大鼠行为学、腰椎间盘形态学、IL-1β阳性表达以及腰大肌被动拉伸张力的变化。结果:模型组与假手术组相比,垂直方向活动度减少(P<0.05),椎间盘纤维环、髓核损伤明显,椎间盘IL-1β免疫组化阳性表达积分光密度增高(P<0.01),腰大肌弹性模量降低(P<0.01);治疗组与模型组比较,椎间盘纤维环及髓核病理变化有所好转,IL-1β免疫组化阳性表达积分光密度降低(P<0.01),腰大肌弹性模量有所提高。结论:前路椎间盘损伤大鼠模型的腰大肌弹性模量有所降低,点拨腰大肌可使其有所恢复,同时可有效改善大鼠椎间盘形态,降低炎性因子IL-1β的表达。

Objective： To observe the passive mechanical properties of psoas major muscles in needling intervertebral disc in- jury rats model and the effects of plucking psoas major muscle on the model. Methods： Male Wistar rats were randomly divided into pseudo--operation group, operation model group and treatment group. L4-5 and LS-6 intervertebral discs were injured by anterior approach in operation model and treatment group, while the same procedure except disc injury was done to pseudo--operation group. For treatment group, bilateral psoas major muscle plucking was done every other day for 10 times. Vertical motion, morphological features and IL-1β positive expression of intervertebral discs, and passive stretching tension of psoas major muscles were observed. Results： Compared with pseudo-operation group, vertical motion reduced significantly （P〈0. 05）, annulus fibrosus, nucleus pulposus injured prominently, IOD of IL-1β positive expression in- creased remarkably （P〈0. 01）, and elastic modulus of psoas major muscles decreased （P〈0. 01） in operation model group. Compared with operation model group, injury of annulus fibrosus and nucleus pulposus became better, IOD of IL-1β positive expression decreased （P〈0.01）, and elastic modulus of psoas major muscles increased in treatment group. Conclusion： After intervertebral disc injury via anterior approach, elastic modulus of psoas major muscles in operation rat models decreased, while psoas major muscles plucking may improve their passive mechanical properties, alleviate the morphological injury of discs, and decrease the positive expression of inflammatory factor IL-1β.