RNA-seq of rat Achilles tendon tissue from pefloxacin and/or dexamethasone treated animals

Tendinopathy is characterized by rupture, pain, or loss of tendon strength. Previous basic and clinical investigations have clarified multiple risk factors, including aging and fluoroquinolone use; however, the etiology remains unclear. We combined real-world data analysis with pharmacological experiments to overcome the gap between basic and clinical research. Analyses of self-reported adverse event databases and the US commercial claims database revealed that dexamethasone prevented fluoroquinolone-induced and age-related tendinopathy. Experimental validation suggested that co-treatment with dexamethasone attenuated pefloxacin-induced mechanical fragility in rat tendons. RNA-seq was conducted to further investigate the molecular mechanism of tendinopathy, focusing on fluoroquinolone.肌腱病（Tendinopathy）以肌腱断裂、疼痛或肌力丧失为核心临床表现。既往基础与临床研究已明确多种致病危险因素，包括衰老与氟喹诺酮类药物（fluoroquinolone）的使用，但该病的病因学机制仍未阐明。为填补基础与临床研究间的研究鸿沟，本研究结合真实世界数据分析与药理学实验展开探究。通过对自我报告不良事件数据库与美国商业理赔数据库的分析，本研究发现地塞米松（dexamethasone）可有效预防氟喹诺酮类药物诱导及衰老相关的肌腱病。实验验证结果表明，联合地塞米松干预可显著减轻培氟沙星（pefloxacin）诱导的大鼠肌腱机械脆性损伤。为进一步探究肌腱病的分子机制，本研究针对氟喹诺酮类药物开展了转录组测序（RNA-seq）分析。