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.