肌腱粘连是手外伤术后的常见问题，迄今仍无有效的解决方法。以往的干预措施抑制外源性机制的同时也抑制了内源性机制，肌腱愈合的强度不够。课题组前期发现miR-29b高表达可以下调TGFβ1和Smad3的蛋白表达，从而防治肌腱粘连，miR-29b inhibitor可逆转此改变。丹参酮ⅡA可以抑制TGF-β1，减少mRNA表达的作用从而防治肌腱粘连。所以我们设想在肌腱断端使用miR-29b inhibitor提前启动内源性修复机制，增生期在腱周组织使用丹参酮ⅡA减少外源性修复机制，在保证肌腱强度的同时，减少了肌腱粘连。从动物实验，体外细胞等不同层次确定：miR-29b inhibitor促进TGF-β1和Smad3的表达，可提前启动内源性修复机制，增强肌腱的强度；miR-29b和丹参酮ⅡA协同作用在TGF-β1/Smad3作用轴上可抑制肌腱粘连。本项目具有较高的创新性，将为肌腱功能修复提供理论支持

Tendon adhesion is a common problem after hand injury, so far there is no effective solution. Previous interventions to suppress exogenous mechanisms also inhibit the endogenous mechanism, tendon healing strength is not enough. The expression of miR-29b can down-regulate the expression of TGFβ1 and Smad3 protein, so as to prevent tendon adhesion, miR-29b inhibitor can reverse this change. Tanshinone Ⅱ A can inhibit TGF-β1, reduce the role of mRNA expression in order to prevent tendon adhesion. Therefore, we envision the use of miR-29b inhibitor at the end of the tendon to initiate an endogenous repair mechanism in advance. The use of tanshinone IIA in the tendon tissue reduces the exogenous repair mechanism and reduces tendon adhesion while ensuring tendon strength. MiR-29b inhibitor promoted the expression of TGF-β1 and Smad3, and could start the endogenous repair mechanism in advance to enhance the strength of tendon. MiR-29b and tanshinone ⅡA synergized in TGF-β1 / Smad3 role in the axis can inhibit tendon adhesion. This project has a high degree of innovation, will provide theoretical support for tendon function repair