Zafirlukast attenuates advanced glycation end-products (AGEs)-induced degradation of articular extracellular matrix (ECM) |
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| Institution: | 1. Department of General Surgery, Fifth Hospital of Wuhan, Wuhan, Hubei 430000, China;2. Department of Hepatobiliary Surgery, Renmin Hospital Hu Bei University of Medicine, Shiyan, Hubei 430000, China;3. Department of Traditional Chinese Medicine, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, China;4. Department of Pharmacy, Fifth Hospital of Wuhan, Wuhan, Hubei 430000, China;5. Department of Geriatrics, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, China;1. Department of orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215000, China;2. Dalian Jiuzhou Century Hospital, Dalian 116400, China;3. Department of Orthopedics, The central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China;4. Department of Internal medicine, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, China;5. Department of orthopedics, Dalian Jiuzhou Century Hospital, Dalian 116400, China;6. Department of orthopedics, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, China |
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| Abstract: | Zafirlukast, a leukotriene receptor antagonist, has been shown to exert a wide range of effects including anti-asthmatic, anti-inflammatory and oral anti-bacterial. Osteoarthritis is one of the most prevalent age-related public health burdens in the modern world. In the present study, we applied zafirlukast in the treatment of human primary chondrocytes and found that it exerts potent anti-osteoarthritic effects. Zafirlukast inhibited AGEs-induced degradation of the articular extracellular matrix by suppressing expression of MMPs, ADAMTS, NOX-4, generation of ROS, and activation of NF-κB via the IκBα/JNK/AP-1 pathway through targeted inhibition of CysLTR1. These findings suggest that zafirlukast possesses a protective effect against AGEs- induced damage and dysfunction in human chondrocytes. |
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