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Heme oxygenase-1 modulates degeneration of the intervertebral disc after puncture in Bach 1 deficient mice

机译:血红素加氧酶-1调节Bach 1缺陷小鼠穿刺后椎间盘退变

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PurposeIntervertebral 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.MethodsCaudal 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.ResultsIn 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.ConclusionsOxidative 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...
机译:目的椎间盘退变被认为是下腰痛的主要特征。此外,氧化应激已被证明是退化性疾病如骨关节炎的重要因素,并且被认为是椎间盘退变的原因。这项研究的目的是澄清使用高表达血红素加氧酶的宽复合体-Tramtrack-Bric-a-brac和cap'n'collar同源性1缺陷(Bach 1?/?)小鼠的氧化应激与椎间盘退变之间的相关性。 -1(HO-1)。 HO-1保护细胞免受氧化应激。方法以12周龄和1岁小鼠的尾椎间盘作为与年龄相关的模型。每组和每个时期,将5只小鼠(总共20只小鼠,总共20张盘)评估为年龄相关模型。 12周大的Bach 1?/?中的C9–C10尾椎间盘使用29号针作为环穿刺模型对野生型小鼠进行穿刺。每组和每个时期,评估5只小鼠(总共60只小鼠,总共60张盘)。在穿刺前,穿刺后1、2、4、8和12周评估椎间盘退变的进展。进行了放射学,组织学和免疫组织学分析以比较Bach 1?/?。结果在与年龄有关的模型中,巴赫1?/?之间没有显着差异。和野生型小鼠的放射学和组织学观察。但是,在环穿刺模型中,组织学评分显示在穿刺后第8周和第12周有显着差异。 HO-1阳性细胞的数目在巴赫1?/?每个时期的老鼠。 Bach 1?/?穿刺后1和2周,细胞凋亡率显着降低。结论预防氧化应激可以避免穿刺后椎间盘的退化过程,减少凋亡细胞的数量。高HO-1表达还可能抑制氧化应激并延迟椎间盘退变的过程...

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