摘要
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-1β) 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-2α 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.
原文 | 英語 |
---|---|
頁(從 - 到) | 15-20 |
頁數 | 6 |
期刊 | Life Sciences |
卷 | 156 |
DOIs | |
出版狀態 | 已發佈 - 7月 1 2016 |
ASJC Scopus subject areas
- 一般藥理學、毒理學和製藥學
- 一般生物化學,遺傳學和分子生物學