血红素加氧酶-1 调节 Bach1 缺陷小鼠椎间盘穿刺后的退变。
Heme oxygenase-1 modulates degeneration of the intervertebral disc after puncture in Bach 1 deficient mice.
机构信息
Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi, Hiroshima, 734-8551, Japan,
出版信息
Eur Spine J. 2012 Sep;21(9):1748-57. doi: 10.1007/s00586-012-2442-5. Epub 2012 Jul 26.
PURPOSE
Intervertebral disc degeneration is considered to be a major feature of low back pain. Furthermore, oxidative stress has been shown to be an important factor in degenerative diseases such as osteoarthritis and is considered a cause of intervertebral disc degeneration. The purpose of this study was to clarify the correlation between oxidative stress and intervertebral disc degeneration using Broad complex-Tramtrack-Bric-a-brac and cap'n'collar homology 1 deficient (Bach 1-/-) mice which highly express heme oxygenase-1 (HO-1). HO-1 protects cells from oxidative stress.
METHODS
Caudal discs of 12-week-old and 1-year-old mice were evaluated as age-related models. Each group and period, 5 mice (a total of 20 mice, a total of 20 discs) were evaluated as age-related model. C9-C10 caudal discs in 12-week-old Bach 1-/- and wild-type mice were punctured using a 29-gauge needle as annulus puncture model. Each group and period, 5 mice (a total of 60 mice, a total of 60 discs) were evaluated. The progress of disc degeneration was evaluated at pre-puncture, 1, 2, 4, 8 and 12 weeks post-puncture. Radiographic, histologic and immunohistologic analysis were performed to compare between Bach 1-/- and wild-type mice.
RESULTS
In the age-related model, there were no significant differences between Bach 1-/- and wild-type mice radiologically and histologically. However, in the annulus puncture model, histological scoring revealed significant difference at 8 and 12 weeks post-puncture. The number of HO-1 positive cells was significantly greater in Bach 1-/- mice at every period. The apoptosis rate was significantly lower at 1 and 2 weeks post-puncture in Bach 1-/- mice.
CONCLUSIONS
Oxidative stress prevention may avoid the degenerative process of the intervertebral disc after puncture, reducing the number of apoptosis cells. High HO-1 expression may also inhibit oxidative stress and delay the process of intervertebral disc degeneration.
目的
椎间盘退变被认为是腰痛的主要特征。此外，氧化应激已被证明是骨关节炎等退行性疾病的一个重要因素，并被认为是椎间盘退变的一个原因。本研究的目的是使用高表达血红素加氧酶-1（HO-1）的 Broad complex-Tramtrack-Bric-a-brac 和 cap'n'collar homology 1 缺陷（Bach 1-/-）小鼠阐明氧化应激与椎间盘退变之间的相关性。HO-1 可保护细胞免受氧化应激。
方法
将 12 周龄和 1 岁龄的小鼠尾椎间盘作为年龄相关模型进行评估。每个组和时期，评估 5 只小鼠（共 20 只小鼠，共 20 个椎间盘）作为年龄相关模型。用 29 号针头对 12 周龄 Bach 1-/-和野生型小鼠的 C9-C10 尾椎间盘进行穿刺，作为环扎穿刺模型。每个组和时期，评估 5 只小鼠（共 60 只小鼠，共 60 个椎间盘）。在穿刺前、1、2、4、8 和 12 周后，对椎间盘退变的进展进行评估。对 Bach 1-/-和野生型小鼠进行放射学、组织学和免疫组织化学分析。
结果
在年龄相关模型中，Bach 1-/-和野生型小鼠在放射学和组织学上无显著差异。然而，在环扎穿刺模型中，组织学评分显示在穿刺后 8 周和 12 周时有显著差异。在每个时期，Bach 1-/-小鼠的 HO-1 阳性细胞数量显著增加。Bach 1-/-小鼠在穿刺后 1 周和 2 周时的细胞凋亡率显著降低。
结论
氧化应激的预防可能会避免穿刺后椎间盘的退行性过程，减少凋亡细胞的数量。高 HO-1 表达也可能抑制氧化应激，延缓椎间盘退变过程。
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