肌腱炎发生率高，常因反复过载牵拉刺激导致且严重影响生活质量，目前机制不明且无特效治疗。HMGB-1与炎症发生的关联目前成为研究热点，但尚无HMGB-1与肌腱炎相关研究。我们前期预实验证实肌腱组织中存在HMGB-1且发现机械过载牵拉可诱导胞内HMGB-1外泌至胞外现象，体内实验重现机械过载牵拉诱发肌腱炎模型中证实组织间HMGB-1含量升高，故提出机械过载刺激诱发肌腱炎是通过HMGB-1外泌再刺激肌腱细胞炎症反应而实现的假说。拟通过体内外确证过载牵拉诱导HMGB-1外泌现象，再体内过表达肌腱中HMGB-1含量对比组织炎症状态明确HMGB-1是调控炎症关键，再体外验证外泌HMGB-1诱发肌腱细胞炎症反应的细胞机制并通过研究NF-κB、MAPK等通路活化情况明确分子机制；最终明确“机械过载-HMGB-1外泌-肌腱炎”假说的机理，增进对肌腱炎发生机制的认识并为后续开发靶向治疗肌腱炎药物提供理论基础。

The incidence of tendonitis is high. It is often caused by repeated mechanical overloading and seriously affect the quality of life. The pathogenesis is not clear while there is no specific treatment. Relation between HMGB-1 and inflammation is popular in recent research, but no publication mentioned HMGB-1 with tendonitis before. Our previous experiments proved HMGB-1 existed in tendon tissue and we also observed that mechanical overloading could induce HMGB-1 released from intracellular to extracellular. In vivo experiment showed that HMGB-1 was increased in the ECM of tendon tissue from the tendonitis/tendinopathy animal model induced by mechanical overloading. So we hypothesize the tendonitis induced by mechanical overloading is mainly resulted by HMGB-1 released to extracellular. We plan to both in Vitro and in Vivo reprove the phenomenon of HMGB-1 release induced by mechanical overloading, and then verify HMGB-1 is the key factor and trigger of tendon tissue inflammation, finally explore the cellular and molecular mechanisms of how released HMGB-1 induces tendon inflammation, especially pays attention to the change of NF-κB pathway and MAPK pathway. Thus to prove our hypothesis and enhance our understanding of the pathogenesis of tendonitis, which can serve as a theoretical underpinning for developing new specific therapy of tendonitis in the further.