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Life Sci ; 156: 15-20, 2016 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-27197027

RESUMO

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 12weeks 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 1week after puncture but did not change in the control group. The interleukin-1 beta (IL-1ß) 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 12weeks 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.


Assuntos
Degeneração do Disco Intervertebral/patologia , Punções , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Colágeno Tipo I/metabolismo , Colágeno Tipo II/metabolismo , Modelos Animais de Doenças , Interleucina-1beta/metabolismo , Degeneração do Disco Intervertebral/metabolismo , Masculino , Metaloproteinase 13 da Matriz/metabolismo , Núcleo Pulposo/metabolismo , Núcleo Pulposo/patologia , Ratos Sprague-Dawley , Cauda , Fatores de Tempo , Fator de Necrose Tumoral alfa/metabolismo , Regulação para Cima
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