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末端病大鼠跟腱超微结构、胶原、MMP-1及TIMP-1的研究 被引量:6

Research on Micro-structure,Collagen,Matrix Metalloproteinase-1 and Tissue Inhibitors of Metalloproteinase-1 in Rats' Achilles Tendon with Enthesiopathy
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摘要 目的:观察末端病大鼠跟腱超微结构、胶原、基质金属蛋白酶1(Matrix metalloproteinase-1,MMP-1)及基质金属蛋白酶抑制剂1(Tissue inhibitors of Metalloproteinase-1,TIMP-1)的变化,探讨跟腱末端病的发病特点。方法:将20只1月龄雄性SD大鼠随机分为对照组和造模组,每组10只。经过5周的电刺激跳跃之后,对实验大鼠跟腱进行HE染色和电镜观察,测试跟腱胶原Ⅰ、胶原Ⅲ、MMP-1及TIMP-1。结果 :与对照组比较,造模组大鼠跟腱胶原排列混乱扭曲,Collagen-Ⅰm RNA的表达和Collagen-Ⅰ蛋白的合成量均显著下降(P<0.05);Collagen-Ⅲm RNA表达迅速上调,Collagen-Ⅲ的合成量也显著增加(P<0.05);MMP-1 m RNA、TIMP-1 m RNA的表达和MMP-1、TIMP-1蛋白含量显著增加(P<0.01)。结论:跟腱末端病发生时,胶原Ⅰ的降解能力增强,胶原Ⅲ的合成能力增强,MMP-1与TIMP-1参与跟腱的重塑。胶原的合成与降解处于动态之中,胶原结构混乱和代谢失衡贯穿于跟腱末端病的整个发病过程。 Objective To study the feature of Achilles enthesiopathy through observing the changes in micro-structure,collagen,matrix metalloproteinase-1(MMP-1)and tissue inhibitors of metalloproteinase-1(TIMP-1)in Achilles tendon with tendinopathy. Methods 20 male SD rats were selected randomly as blank group(n = 10)and model group(n = 10). Rats in the model group were forced to jump 20 minutes twice with an interval of 10 minutes a day for a total of 5 weeks. The Achilles tendon of the rats in two groups were observed,and the collagen-I,collagen-III,MMP-1 and TIMP-1 were tested. Results Compared with the blank group,the tendon collagen was disorganized and twisted,the expression of collagen-I m RNA and collagen-I decreased significantly(P 〈 0.05),collagen-III m RNA and collagenIII increased significantly(P 〈 0.05),and MMP-1 m RNA,TIMP-1 m RNA,MMP-1,and TIMP-1increased significantly in model group(P 〈 0.01). Conclusion The degradation ability of collagen-I and synthesis ability of collagen-III enhanced in Achilles of rats with enthesiopathy,at the same time MMP-1 and TIMP-1 took part in the remodeling of Achilles tendon.
出处 《中国运动医学杂志》 CAS CSCD 北大核心 2014年第9期902-906,922,共6页 Chinese Journal of Sports Medicine
关键词 末端病 跟腱 超微结构 胶原 基质金属蛋白酶1 基质金属蛋白酶抑制剂1 enthesiopathy Achilles tendon micro-structure collagen MMP-1 TIMP-1
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二级参考文献87

共引文献41

同被引文献92

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