1. 腿止点过度使用性损伤形成过程中细胞外基质的调节机制.
- Author
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陈晓世, 梁孝天, 张于, 刘海涛, 曲艺, 王博, and 王琳
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COLLEGE sports , *COLLAGEN , *CONTROL groups , *PLYOMETRICS , *TENDINOSIS , *OVERUSE injuries , *BIOPROSPECTING - Abstract
BACKGROUND: Overuse tendinopalhy is a common disease with no ideal treatment because the pathnogensis of tendinopathy is still unclear. OBJECTIVE: To explore the effects of enzymes effecting collagen synthesis on the metabolism of collagen I and collagen Ill during load accumulation in a model of patella-patellar tendon junction rweruse injury. METHODS: Thirty-two adult female New Zealand wihite rabbits were randomly divided into a jumping group (n=16) and a control group (n=16). In the jump group, rabbits were subjected to jump training for 2, 4, 6, and 8 weeks, 150 jumps per day, 5 days per week. No intervention was performed in the control group. Bilateral patella-patellar tendon junction samples were taken at 24 hours after 2-, 4-, 6-, and 8- week training. The time-series changes of matrix metalloproteinase 1 (MMP1), tissue inhibitor of metelloproteinase 1 (T IMP1), collagen I, and collagen Ill ware measured by immunohistochemistry. The study was performed with an ethic approval from the Animal Ethical Committee of Be jing Sport University, China (approval No. BSU2015022). RESULTS AND CONCLUSION: Compared with the control group, the MMP1 activity was significantly lower within the first 6 weeks of training, TIMP1 activity was significantly higher at 4-8 weeks of training, and TIMP1/MMP1 was significantly higher at 4-8 weeks of training. Compared with the control group, the expression of collagen I was significantly increased in the first 6 weeks of training, but the expression of collagen Ill was significantly lowered after 8 weeks of training. TIMP1 activity was significantly positively correlated with collagen I expression, and MMP1 activity was significantly negatively correlated with collagen I expression. To conclude, the patella-patellar tendon junction, during jumping load accumulation, mainly responded to load stimulation by increasing collagen I expression. In the first 2 weeks of load accumulation, the expression of collagen I was mainly increased by inhibiting MMP1 activity; in the period of 4 to 6 weeks of load accumulation, the expression of collagen I was mainly increased by increasing the activity of TIMP1 and inhibiting the activity of MMP1; and after 8 weeks of load accumulation, TIMP1 could promote collagen synthesis but with inability to antagonize the degradation of collagen I and Ill by MMP1 . Then the expression of collagen I decreased from the peak level after 6 weeks of training to the control group level, and the level of collagen Ill decreased to be less than the level of the control group. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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