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The pathological changes of chondrocytes involve oxidative stress, the pro\u2010inflammatory response, and pro\u2010apoptotic events. Galectin\u20103 (Gal\u20103) is a 35\u2009kDa protein with a special chimeric structure. Gal\u20103 participates in the progression of many diseases, such as cancer metastasis and heart failure. A previous study demonstrated that Gal\u20103 expression in human cartilage with OA is increased. However, the role of Gal\u20103 in chondrocyte dysfunction in joints is still unclear. In this study, we applied Gal\u20103 (5\u201320\u2009\u03bcg\/ml) to TC28a2 human chondrocyte cells for 24\u2009h to induce chondrocyte dysfunction. We found that Gal\u20103 upregulated TLR\u20104 and MyD88 expression and NADPH oxidase, thereby increasing intracellular ROS in the chondrocytes. Gal\u20103 increased phosphorylated MEK1\/2 and ERK levels, and promoted NF\u2010\u03baB activity. This activation of NF\u2010\u03baB was reduced by silencing TLR\u20104 and NOX\u20102. In addition, Gal\u20103 caused apoptosis of chondrocytes through the mitochondrial\u2010dependent pathway via the TLR\u20104\/NADPH oxidase\/MAPK axis. Our study proves the pathogenic role of Gal\u20103 in Gal\u20103\u2010induced chondrocyte dysfunction and injuries.<\/jats:p>","DOI":"10.1002\/tox.23414","type":"journal-article","created":{"date-parts":[[2021,12,11]],"date-time":"2021-12-11T16:53:55Z","timestamp":1639241635000},"page":"478-488","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Galectin\u20103 facilitates inflammation and apoptosis in chondrocytes through upregulation of the <scp>TLR<\/scp>\u20104\u2010mediated oxidative stress pathway in <scp>TC28a2<\/scp> human chondrocyte cells"],"prefix":"10.1002","volume":"37","author":[{"given":"Wan\u2010Ching","family":"Chou","sequence":"first","affiliation":[{"name":"Department of Physical Therapy, College of Medicine National Cheng Kung University  Tainan 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