Tendinopathy is a common problem in sports medicine which can lead to severe morbidity. Aspirin, as the classical representative of non‐steroidal anti‐inflammatory drugs (NSAIDs) for its anti‐inflammatory and analgesic actions, has been commonly used in treating tendinopathy. While its treatment effects on injury tendon healing are lacking, illuminating the underlying mechanism may provide scientific basis for clinical treatment.

Firstly, we used immunohistochemistry and qRT‐PCR to detect changes in CD14, CD206, iNOS, IL‐6, IL‐10, MMP‐3, TIMP‐3, Col‐1a1, biglycan, Comp, Fibronectin, TGF‐β1，ACAN，EGR‐1 and FMOD. Next, Western blot was used to measure the protein levels (IL‐6, IL‐10, TGF‐β1, COMP, TIMP‐3, STAT‐3/P‐STAT‐3 and JNK/P‐JNK) in TSCs. Then, migration and proliferation of TSCs were measured through wound healing test and BrdU staining. Finally, the mechanical properties of injury tendon were detected.

After aspirin treatment, the inflammation and scar formation in injury tendon were significantly inhibited by aspirin. Still, tendon's ECM was positively balanced. Increasing migration and proliferation ability of TSCs induced by IL‐1β were significantly reversed. JNK/STAT‐3 signalling pathway participated in the process above. In addition, biomechanical properties of injury tendon were significantly improved.

Taken together, the findings suggested that aspirin inhibited inflammation and scar formation via regulation of JNK/STAT‐3 signalling and decreased rerupture risk of injury tendon. Aspirin could be an ideal therapeutic strategy in tendon injury healing.

Tendons are connective tissues which attach muscle to bone and carry mechanical force, permitting joint and whole body movement. Repeated over mechanical force loading leads to tendinopathy, which is characterized as imbalance between micro‐tear and repair in tendon. Studies have reported that tendinopathy covers about 30% of sports injuries and its pathogenesis is highly related to inflammation and degradation of connective tissue. Inflammation is a starter and necessary for injury tissue healing process, which may generate scar formation in the injury site. At the same time, scar formation may increase the fragility of tendon, which may induce risk of tendon rupture. Based on this, it is important to treat tendinopathy in anti‐inflammation and inhibiting scar healing process.

NSAIDs inhibit the inflammation and relieve pain through inhibiting prostaglandin. Aspirin, one of the most commonly used NSAIDs for over 150 years, has been recently used to display multiple effects such as antipyretic, analgesic in cardiovascular system, central nervous system and some cancers. Though aspirin has been used to treat tendinopathy, evidence for this treatment is lacking, especially its effect on tendon regeneration healing.

In response to micro‐damage of tendinopathy, tissues adjacent to the injury area initiate a cascade of inflammation and repair events that are necessary to restore tissue integrity and function. Some reports have pointed out that inflammation reaction has run through the whole process of tissue repair and has played the role like a double sword.On the one hand, inflammation can induce wound healing and closing through fibrosis and scar formation and prevent wound infection; on the other hand, inflammation‐induced scar healing can hamper tissue regeneration and further may reduce the function of tissue or organ. Inflammation is bound to affect tendon extracellular matrix (ECM). Anomalies in the ECM composition of the scar tissue after tendon injury may contribute to a poor and delayed regeneration healing process resulting in compromised tissue quality for example, dexamethasone‐induced spontaneous tendon rupture and dexamethasone‐decreased self‐repair capability are very common in clinical practice. TSCs or progenitor cells were reported firstly in human and mouse tendons in 2007 and were confirmed subsequently in rat and rabbit tendons. TSCs differed from tenocytes in terms of their colony‐forming ability, self‐renewal ability and multi‐differentiation potential, which enable them to differentiate into tenocytes, adipocytes, chondrocytes and osteocytes, so the viability and tenogenic differentiation of TSCs are tightly associated with the maintenance of the tendon microenvironment and the development of tendinopathy.

The present study aimed to make clear that the effect of aspirin on TSCs viability in vitro, inflammation and regeneration healing process of tendinopathy and the mechanical properties of the injury tendon, and to provide new therapeutic knowledge of aspirin treatment on tendon injury.

Thanks & Regards,

ALPINE

Managing Editor

 Journal of Orthopaedics and Trauma

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