School of Physical Education, Henan University, Kaifeng, China.
School of Sports Medicine and Physical Therapy, Beijing Sports University, Beijing, China.
Am J Sports Med. 2020 Apr;48(5):1141-1150. doi: 10.1177/0363546520902447. Epub 2020 Feb 19.
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.
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.
Controlled laboratory study.
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.
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 ( < .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 ( < .01).
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.
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.
过度使用导致髌腱纤维化的发病机制尚不清楚。为了进一步研究过度使用导致髌腱纤维化的有效治疗方法，有必要构建一种可靠的动物模型。
采用电刺激诱发跳跃的方法建立兔髌腱纤维化模型，探讨该模型髌腱纤维化的发生发展过程。
对照实验研究。
32 只新西兰大白兔随机分为跳跃组和对照组，对照组不做任何处理，跳跃组每天跳跃 150 次，每周 5 天。在治疗开始后 2、4、6、8 周，每组各取 4 只兔的髌腱，进行苏木精-伊红染色、免疫组化染色和实时聚合酶链反应，评估跳跃训练对髌腱组织学和纤维化相关因子表达的影响。
跳跃组髌腱纤维化的组织学变化在第 4 周最为明显。与相应时间点的对照组相比，跳跃训练 4 周后髌腱中 TGF-β1、CTGF、COL-I 和 COL-III 的 mRNA 和蛋白表达显著上调（ <.05）。组内不同时间点比较，跳跃组 TGF-β1、COL-I 和 COL-III 的 mRNA 和蛋白表达在第 4 周最高（ <.01）。
过度使用导致髌腱发生纤维化，且 4 周时变化最明显。跳跃负荷增加了髌腱中 TGF-β1 和 Smad3 的分泌，CTGF 上调，COL-I 和 COL-III 合成增加，被认为是纤维化的发病机制。
本研究模拟了不同时间点跳跃负荷对肌腱纤维化的影响，确定了兔模型中跳跃训练与髌腱纤维化之间的时间进程关系，为髌腱纤维化的研究提供了新的动物模型。
