屈指肌腱愈合时，内源性愈合延迟，外源性粘连形成，严重影响手指功能。我们前期课题发现，TGF-β3作为TGF-β1的天然拮抗剂，TGF-β3组织工程滑膜鞘有良好的抗粘连作用。近来研究发现，cAMP反应序列结合蛋白（CREB-1）与TGF-β3启动子结合调节内源性TGF-β3表达。我们新近发现，周期性机械牵伸下，肌腱内源性愈合处TGF-β3和CREB表达增加。因此，我们预测机械牵伸下CREB/TGF-β3信号通路参与介导肌腱内源性愈合。本课题拟在周期性机械牵伸下，检测肌腱、滑膜鞘TGFβ3、CREB及Smad的分布规律；通过CREB基因过表达和干扰抑制，分别检测其肌腱细胞外基质、TGFβ3、胶原等表达影响；通过肌腱Scx-Cre转基因动物检测，CREB诱导TGFβ3分泌促肌腱内源性愈合的作用；探讨CREB对肌腱细胞内源性TGFβ3自反馈分泌的机制。本项目将为促肌腱内源性愈合抗粘连提供新的依据。

In flexor tendon healing, delayed endogenous healing and exogenous adhesion formation can seriously affect the function of the fingers. Our previous study found that TGF- beta 3 as a natural antagonist of TGF- beta 1 and TGF- beta 3 tissue engineering synovial sheath has good anti-adhesion effects. Recently, it has been found that cAMP binding protein (CREB-1) and TGF- beta 3 promoter regulate the expression of endogenous TGF- beta 3. We recently found that under periodic mechanical stretching, TGF-beta3 expression and CREB increased in tendon endogenous healing site. Therefore, we predict under mechanical stretch TGF-beta3/CREB signaling pathway mediate tendon endogenous healing. This research aims to test distribution of TGF beta 3, CREB and Smad in tendon and synovial sheath under periodic mechanical stretch; through the CREB gene expression and interference suppression, we respectively can detect the tendon extracellular matrix, TGF beta 3, collagen expression. Using tendon Scx-Cre transgenic animal, we can test that CREB induces TGF beta 3 secretion to promote tendon endogenous healing. At the same time, the mechanism of self feedback of CREB to promote TGF beta 3 secretion on endogenous tendon cell will be investigated. This project will provide a new theoretical basis for endogenous tendon healing and anti-adhesion.