Time course investigation of intervertebral disc degeneration in a rat-tail puncture model
Time course investigation of intervertebral disc degeneration in a rat-tail puncture model
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DOI：
10.1016/j.lfs.2016.05.020
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发表时间：
2016-07-01
期刊：
影响因子：
6.1
通讯作者：
Tsai, Tung-Hu
中科院分区：
文献类型：
--
作者：
Chen, Chia-Hsian;Chiang, Chang-Jung;Tsai, Tung-Hu
目的：椎间盘退变被认为是导致下腰痛的原因之一。本研究旨在探讨针刺致大鼠IVD退变的发病机制及其调控机制。主要方法：采用克氏针和自制栓子制作大鼠尾部穿刺克氏针模型。分别于术后0.5、1、2、6、12周通过组织学检查和I型、II型胶原等因子表达的定量测定来评价椎间盘退变的进展情况，并与同龄对照组大鼠进行比较。基质金属蛋白酶13(MMP13)在穿刺术后1周升高，而对照组无明显变化。白细胞介素1β(IL-1β)在急性期的表达水平明显高于对照组。低氧诱导因子2(HIF-2)在针刺组表达增加。此外，与邻近的非穿刺节段相比，HIF-2α在髓核中的表达水平在穿刺后即刻短暂升高，然后下降，并在穿刺后12周升高。意义：在这种鼠尾穿刺法模型中观察到的退变变化类似于人类腰椎间盘退变，该模型可能对阐明腰椎间盘退变的分子机制和途径有价值。(C)2016 Elsevier Inc.保留所有权利。
Aims: Intervertebral disc (IVD) degeneration was believed to contribute to lower back pain. The aim of the study was to investigate the pathogenesis and regulatory mechanism of puncture-induced IVD degeneration.Main methods: We established a rat-tail puncture model using Kirschner wire and a homemade stopper. The progress of disc degeneration was evaluated by histological examination and the quantitative measurement of type I, type II collagen and other factors expression at 0.5, 1, 2, 6, and 12 weeks after puncture and was compared with control rats of the same age.Key findings: Histological examination and Safranin-O staining revealed progressive degeneration of the punctured disc. Matrix metalloproteinase 13 (MMP13) was increased at 1 week after puncture but did not change in the control group. The interleukin-1 beta (IL-1 beta) mRNA expression level was elevated at the acute stage after puncture compared with the control group. The hypoxia inducible factor 2 (HIF-2) increased expression in punctured groups. Additionally, compare to adjacent non-punctured segments, HIF-2 alpha expression level transiently increased and then decreased in the nucleus pulposus immediately following puncture, and it then increased 12 weeks after puncture.Significance: The degenerative changes observed in this rat-tail puncture model are similar to human disc degeneration and that this model may be valuable for elucidating the molecular mechanisms and pathways underlying disc degeneration. (C) 2016 Elsevier Inc. All rights reserved.