Aspirin inhibits inflammation and scar formation in the injury tendon healing through regulating JNK/STAT-3 signalling pathway
Aspirin inhibits inflammation and scar formation in the injury tendon healing through regulating JNK/STAT-3 signalling pathway
复制标题
阿司匹林通过调节JNK/STAT-3信号通路抑制损伤肌腱愈合过程中的炎症和疤痕形成。
DOI：
10.1111/cpr.12650
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发表时间：
2019-07-01
影响因子：
8.5
通讯作者：
Tang, Kanglai
中科院分区：
文献类型：
--
作者：
Wang, Yunjiao;He, Gang;Tang, Kanglai
客观上肌腱病是运动医学中常见的问题，可导致严重的发病率。阿司匹林作为非甾体抗炎药的经典代表，具有抗炎、镇痛作用，常用于肌腱病的治疗。但其对损伤肌腱愈合的治疗作用尚不明确，阐明其作用机制可为临床治疗提供科学依据。材料与方法首先采用免疫组化和qRT-PCR方法检测CD 14、CD 206、iNOS、IL-6、IL-10、MMP-3、TIMP-3、Col-1a 1、biglycan、Comp、Fibronectin、TGF-β 1？禁毒办？EGR-1和FMOD。接着，使用蛋白质印迹法测量TSC中的蛋白质水平（IL-6、IL-10、TGF-β 1、COMP、TIMP-3、STAT-3/P-STAT-3和JNK/P-JNK）。通过伤口愈合实验和BrdU染色检测TSCs的迁移和增殖情况。最后对损伤肌腱的力学性能进行检测。结果阿司匹林能明显抑制损伤肌腱的炎症反应和瘢痕形成。尽管如此，肌腱的ECM是积极的平衡。IL-1 β诱导的TSCs迁移和增殖能力的增加被显著逆转。JNK/STAT-3信号通路参与了上述过程。此外，损伤肌腱的生物力学性能也得到明显改善。结论阿司匹林通过调控JNK/STAT-3信号通路抑制炎症反应和瘢痕形成，降低损伤肌腱再断裂风险。阿司匹林可能是肌腱损伤愈合的理想治疗策略。
Objectively 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. Materials and methods 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-beta 1?ACAN?EGR-1 and FMOD. Next, Western blot was used to measure the protein levels (IL-6, IL-10, TGF-beta 1, 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. Results 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-1 beta were significantly reversed. JNK/STAT-3 signalling pathway participated in the process above. In addition, biomechanical properties of injury tendon were significantly improved. Conclusions 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.