Antioxidant treatment with vitamin C attenuated rotator cuff degeneration caused by oxidative stress in Sod1-deficient mice.
Antioxidant treatment with vitamin C attenuated rotator cuff degeneration caused by oxidative stress in Sod1-deficient mice.
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DOI：
10.1016/j.jses.2017.11.003
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发表时间：
2018-03-01
期刊：
影响因子：
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通讯作者：
Shimizu, Takahiko
中科院分区：
文献类型：
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作者：
Morikawa, Daichi;Nojiri, Hidetoshi;Shimizu, Takahiko
背景技术背景：肩袖退变是导致肩袖撕裂的几个因素之一;然而，这种退变的机制仍不清楚。我们以前报道过，缺乏抗氧化酶，超氧化物歧化酶1（SOD 1），在小鼠中诱导冈上肌腱附着点，复制人类肩袖退化的模型退化。在这项研究中，我们分析了可能的影响，维生素C（VC），一种主要的抗氧化剂，在Sod 1-/- mice.METHODS的冈上肌附着点的退行性变化：我们管理的VC或车辆，蒸馏水，为8周的Sod 1-/-和野生型雄性小鼠开始在12周龄（n=5-8每组）。当小鼠20周龄时，我们切片肩袖组织样本，并进行苏木精-伊红和甲苯胺蓝染色定量组织学evaluation.Results：VC管理，与车辆管理相比，衰减的组织学变化，包括错位的4层结构，碎片潮标，甲苯胺蓝染色，在冈上肌附着点的Sod 1-/-小鼠。在定量组织学评价中，所有参数均显着下降，在Sod 1-/-小鼠与野生型小鼠相比，除了nonchondrocytes.CONCLUSION的数量：我们表明，抗氧化剂治疗，VC管理，衰减肩袖变性，类似于在人类中观察到的，这是由氧化应激Sod 1-/-小鼠。VC效应包括定量组织学参数和其他组织学变化的改善。这些结果表明，VC治疗可以防止氧化应激引起的肩袖退变。
BACKGROUND: Rotator cuff degeneration is 1 of several factors that lead to rotator cuff tears; however, the mechanism of this degeneration remains unclear. We previously reported that deficiency of an antioxidant enzyme, superoxide dismutase 1 (Sod1), in mice induced degeneration in supraspinatus tendon entheses, a model that replicates human rotator cuff degeneration. In this study, we analyzed possible effects of vitamin C (VC), a major antioxidant, on the degenerative changes of supraspinatus entheses in Sod1 -/- mice.METHODS: We administered VC or vehicle, distilled water, for 8 weeks to Sod1 -/- and wild-type male mice beginning at 12 weeks of age (n=5-8 per group). When mice were 20 weeks of age, we sectioned rotator cuff tissue samples and performed hematoxylin-eosin and toluidine blue staining for quantitative histologic evaluation.RESULTS: VC administration, compared with vehicle administration, attenuated the histologic changes, including a misaligned 4-layered structure, fragmented tidemark, and toluidine blue staining, in the supraspinatus entheses of Sod1 -/- mice. In the quantitative histologic evaluation, all parameters were significantly decreased in Sod1 -/- mice compared with wild-type mice, except for the number of nonchondrocytes.CONCLUSION: We demonstrated that an antioxidant treatment, VC administration, attenuated the rotator cuff degeneration, similar to that observed in humans, that is caused by oxidative stress in Sod1 -/- mice. VC effects included improvements in quantitative histologic parameters and other histologic changes. These results suggest that VC treatment can prevent oxidative stress-induced degeneration of the rotator cuff.