轴向负载诱导肾虚小鼠椎间盘退变的实验研究

Experimental Study on the Intervertebral Disc Degeneration Induced by Spinal Axial Loading in Mice with Kidney Deficiency

目的:探究采用自制的热板鼠笼诱导的间断轴向力学负载环境对肾虚小鼠腰椎间盘退变的影响。方法:选择16个月龄老年小鼠36只,随机分为对照组、模型组及肾虚模型组,每组12只。每日于固定时间段将肾虚模型组及模型组小鼠放入自制的热板鼠笼,开始跳跃后计时10 min,对照组小鼠不予处理。分别在造模1个月和3个月后,通过HE、ABH染色分别比较三组小鼠腰椎间盘组织学差异,通过免疫组化测定Ⅱ型胶原来说明三组小鼠椎间盘退变的不同情况。结果:染色结果表明模型组和肾虚模型组小鼠椎间盘高度明显小于对照组,模型组与肾虚模型组样本软骨终板都存在更严重的骨化,模型组较对照组明显。模型组与肾虚模型组椎间盘内软骨老化较对照组明显升高,且肾虚模型组髓核的软骨细胞退变作用更为严重,其阳性染色较模型组有明显的升高。结论:间断的轴向力学负载能够促进小鼠椎间盘内软骨细胞退变和基质分解酶的表达,从而诱导小鼠腰椎间盘退变的发生和发展,且其对肾虚小鼠腰椎间盘能造成更为严重的椎间盘退变。

Objective:To investigate the efficacy of intermittent spinal axial mechanical loading induced by self-made hot plate cage on lumbar intervertebral disc degeneration in mice with kidney deficiency.Methods:Thirty-six 16 months-old mice were randomly divided into kidney deficiency model group,model group and control group with 12 mice in each group.The mice of kidney deficiency model group and model group were put into the self-made hot-plate cage at the same time every day,the control group was not treated.Histological differences of lumbar intervertebral disc in three groups were compared by HE and ABH staining,and the typeⅡCollagen was detected by immunohistochemistry to explain the different conditions of intervertebral disc degeneration in the three groups of mice after modeling for 1 month and 3 months respectively.Results:The results of staining showed that the height of intervertebral disc in model group and kidney deficiency model group was significantly lower than that in control group.The cartilage endplates in the model group and the kidney deficiency model group were more ossified than those in the control group.The aging of intervertebral disc cartilage in model group and kidney-deficiency model group was higher than that in control group,and the degeneration of nucleus pulposus in kidney-deficiency model group was more serious,and the positive staining was higher than that in model group.Conclusion:Intermittent spinal axial mechanical loading can promote the degeneration of chondrocyte and increase expression of decomposing enzyme in intervertebral disc of mice,which induce the initiation and development of lumbar disc degeneration in mice.And it can cause more serious intervertebral disc degeneration in kidney deficiency mice.