CAJ | 학술논문

为研究生长因子在过度使用导致肌腱退行性变中的作用机制,利用SD大鼠8周下坡跑模型造成肱二头肌长头肌腱结节沟段退行性变,采用免疫组织化学等方法,检测运动各阶段肌腱IGF1、TGFβ1、BMP12、bFGF蛋白表达情况。结果：在肱二头肌长头整体肌腱中,只有bFGF表达显著增加;bFGF在过度使用第2周显著升高（P〈0.01）,第4周下降,第6周（P〈0.05）和第8周（P〈0.01）再次持续升高。在肱二头肌长头肌腱结节沟段,IGF1表达无显著变化,TGFβ1、bFGF、BMP12表达均显著增高;TGFβ1表达逐渐升高,第6周达到高峰（P〈0.05）,第8周迅速下降;bFGF表达在第4周迅速升高到峰值（P〈0.01）,然后下降,到第8周与对照组无显著差异;BMP12蛋白表达逐渐增加,第6周达到高峰（P〈0.05）,第8周略下降。结论：肌腱过度使用中相关生长因子蛋白长期异常表达是肌腱退行性变的重要病理变化,有可能推动了肌腱退行性变的进程。
위연구생장인자재과도사용도치기건퇴행성변중적작용궤제,이용SD대서8주하파포모형조성굉이두기장두기건결절구단퇴행성변,채용면역조직화학등방법,검측운동각계단기건IGF1、TGFβ1、BMP12、bFGF단백표체정황。결과：재굉이두기장두정체기건중,지유bFGF표체현저증가;bFGF재과도사용제2주현저승고（P〈0.01）,제4주하강,제6주（P〈0.05）화제8주（P〈0.01）재차지속승고。재굉이두기장두기건결절구단,IGF1표체무현저변화,TGFβ1、bFGF、BMP12표체균현저증고;TGFβ1표체축점승고,제6주체도고봉（P〈0.05）,제8주신속하강;bFGF표체재제4주신속승고도봉치（P〈0.01）,연후하강,도제8주여대조조무현저차이;BMP12단백표체축점증가,제6주체도고봉（P〈0.05）,제8주략하강。결론：기건과도사용중상관생장인자단백장기이상표체시기건퇴행성변적중요병리변화,유가능추동료기건퇴행성변적진정。
Objective：This experiment was designed to study the role of growth factors in tendon degeneration overuse-induced.Methods：This study established the rats tendon overused model by downhill running,detected growth factors gene expression in various stages of overuse by immunohistochemistry.Results：In whole tendon,bFGF protein expression was significantly increased during the downhill running,but TGFβ1,bFGF and BMP12 had no significantly change.bFGF was significantly increased at 2 weeks（P〈0.01）,decreased at 4 weeks,and raised again at 6-8 weeks.In rat biceps brachii tendon intertubercular sulcus parts,IGF1 expression had no significantly change,but expression of TGFβ1,bFGF,and BMP12 were significantly increased.The expression of TGFβ1increased gradually,reached a peak at 6weeks（P〈0.05）,decreased rapidly at 8 weeks.The expression of bFGF reached the peak at 4 weeks value（P〈0.01）,and then decreased at 8 weeks.The expression of BMP12 protein increased gradually,reached a peak at 6 weeks（P〈0.05）,and declined slightly at 8 weeks.Conclusion：During overuse process,long-term abnormal expression of growth factors was an important pathological chang of tendon degeneration,which probably pushed the tendon degeneration process.