当前位置:主页 > 医学论文 > 外科论文 >

张力载荷诱导下兔椎间盘退变体内模型的建立及意义

发布时间:2018-09-19 13:28
【摘要】:背景:异常应力被认为是导致椎间盘退变的重要因素。随着对椎间盘退变发生机制研究的不断深入,建立一种理想的力学相关性椎间盘退变体内动物模型具有重要的实践意义。目的:建立兔椎间盘体内模型,施以持续的张力载荷,探究其对椎间盘退变的影响。方法:25只6月龄新西兰大白兔随机分为3组,空白对照组5只,假加力组10只,加力组10只。空白对照组不作任何处理,于实验第1天手术获取L_(4/5)椎间盘;加力组和假加力组均固定椎间盘加力器,加力组施以L_(4/5)椎间盘1 MPa(10 kg/cm~2)轴向牵张力,假加力组仅固定加力器但不加力,2组分别在14,28 d手术获取椎间盘。X射线观察L_(4/5)椎间隙高度变化和邻近骨质改变;苏木精-伊红染色观察椎间盘组织形态学变化;NBT染色观察椎间盘细胞存活状态;RT-PCR检测各时间点椎间盘组织中蛋白聚糖、Ⅱ型胶原和SOX9 m RNA表达变化。结果与结论:(1)假加力组各时间点与空白对照组相比,X射线表现、苏木精-伊红染色、细胞存活状态和蛋白多糖、Ⅱ型胶原、SOX9 m RNA表达差异均无显著性意义;(2)与空白对照组相比发现,加力组随着张力载荷时间的延长,L_(4/5)椎间隙逐渐变窄,关节面毛糙,上下椎体前缘骨质增生呈唇状改变;椎间盘细胞分布不均匀、紊乱;髓核脱水缩小,纤维环排列混乱,脊索细胞空泡状组织趋于消失;蛋白多糖、Ⅱ型胶原、SOX9表达显著下调;(3)结果提示,成功建立了兔椎间盘体内模型,并在此模型基础上阐明持续张力载荷可直接导致椎间盘退变。
[Abstract]:Background: abnormal stress is considered to be an important factor leading to disc degeneration. With the further study of the mechanism of disc degeneration, it is of great practical significance to establish an ideal animal model of intervertebral disc degeneration in vivo. Aim: to establish a model of intervertebral disc in rabbits and to investigate the effect of continuous tension load on the degeneration of intervertebral disc. Methods Twenty five 6 months old New Zealand white rabbits were randomly divided into 3 groups: blank control group (n = 5), sham exertion group (n = 10) and postconditioning group (n = 10). The blank control group received L4 / 5 intervertebral disc without any treatment on the first day of the experiment, and the L _ (4 / 5) intervertebral disc axial tension of 1 MPa (10 kg/cm~2) was applied to the control group. In the sham exertion group, the height of L4 / 5 intervertebral space and the changes of adjacent bone were observed at 1428 d after operation. Histomorphologic changes of intervertebral disc were observed by hematoxylin and eosin staining. The expression of proteoglycan, type 鈪,

本文编号:2250260

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/waikelunwen/2250260.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户ea860***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com