BACKGROUND The pathogenesis of patellar tendon fibrosis caused by overuse remains unclear. In an effort to further investigate effective treatments for patellar tendon fibrosis attributed to overuse, it is necessary to construct a reliable animal model. PURPOSE A rabbit patellar tendon fibrosis model was developed with the use of electrical stimulation to induce jumping. The pathogenesis and development of patellar tendon fibrosis were subsequently investigated with this model. STUDY DESIGN Controlled laboratory study. METHODS A total of 32 New Zealand White rabbits were randomly divided into a jumping group and a control group. Rabbits in the control group did not receive any treatment, while those in the jumping group jumped 150 times daily, 5 days per week. At 2, 4, 6, and 8 weeks after the initiation of treatment, the patellar tendons of 4 rabbits from each group were harvested and subjected to hematoxylin and eosin staining, immunohistochemical staining, and real-time polymerase chain reaction. The influence of jumping training on the expressions of histology- and fibrosis-related factors in the patellar tendon was assessed. RESULTS The histological changes of patellar tendon fibrosis in the jumping group were most pronounced at 4 weeks. When compared with the control group at corresponding time points, the mRNA and protein expressions of TGF-β1, CTGF, COL-I, and COL-III were upregulated significantly in the patellar tendon after jumping training for 4 weeks (P < .05). Intragroup comparison at different time points indicated that the mRNA and protein expressions of TGF-β1, COL-I, and COL-III were the highest at 4 weeks in the jumping group (P < .01). CONCLUSION It was found that patellar tendon fibrosis occurred because of overuse and the peak changes occurred at 4 weeks. Jumping load increased the secretions of TGF-β1 and Smad3 in the patellar tendon, with CTGF upregulation and higher synthesis of COL-I and COL-III, which were considered the pathogenesis of fibrosis. CLINICAL RELEVANCE This study simulated the effects of jumping load on tendon fibrosis at different time points. Moreover, the time course relationship between jumping training and patellar tendon fibrosis in the rabbit model was determined, which provided a new animal model for the study of patellar tendon fibrosis.

中文翻译：

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兔子过度使用模型中Pat骨肌腱纤维化的发病机制和发展。

背景技术由过度使用引起的pa肌腱纤维化的发病机制仍不清楚。为了进一步研究有效治疗过度使用引起的pa腱纤维化的方法，有必要构建一个可靠的动物模型。目的建立兔pa肌腱纤维化模型，利用电刺激诱发跳跃。随后用该模型研究了tend腱纤维化的发病机制和发展。研究设计受控的实验室研究。方法将32只新西兰白兔随机分为跳跃组和对照组。对照组的兔子没有接受任何治疗，而跳跃组的兔子则每天，每周5天跳150次。在开始治疗后的2、4、6和8周，收集每组四只兔的tell腱，进行苏木精和曙红染色，免疫组织化学染色和实时聚合酶链反应。评估了跳跃训练对pa腱中组织学和纤维化相关因子表达的影响。结果跳跃组of肌腱纤维化的组织学变化在第4周最为明显。与对照组相比，在跳跃训练4周后the骨肌腱中TGF-β1，CTGF，COL-I和COL-III的mRNA和蛋白表达显着上调（P <.05） 。在不同时间点进行的组内比较表明，在跳跃组中，TGF-β1，COL-1和COL-III的mRNA和蛋白表达在4周时最高（P <。01）。结论发现pa肌腱纤维化是由于过度使用引起的，并且峰值变化发生在第4周。跳跃负荷增加了tell骨肌腱中TGF-β1和Smad3的分泌，CTGF上调以及COL-I和COL-III的较高合成被认为是纤维化的发病机理。临床相关性这项研究模拟了跳跃负荷在不同时间点对肌腱纤维化的影响。此外，确定了跳跃训练与jumping骨肌腱纤维化之间的时程关系，为研究pa骨肌腱纤维化提供了新的动物模型。CTGF的上调和COL-I和COL-III的较高合成被认为是纤维化的发病机理。临床相关性这项研究模拟了跳跃负荷在不同时间点对肌腱纤维化的影响。此外，确定了跳跃训练与jumping骨肌腱纤维化之间的时程关系，为研究pa骨肌腱纤维化提供了新的动物模型。CTGF的上调和COL-I和COL-III的较高合成被认为是纤维化的发病机理。临床相关性这项研究模拟了跳跃负荷在不同时间点对肌腱纤维化的影响。此外，确定了跳跃训练与jumping骨肌腱纤维化之间的时程关系，为研究pa骨肌腱纤维化提供了新的动物模型。