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Excessive oxidative stress is another central driver of OA pathogenesis, amplifying inflammation and accelerating chondrocyte apoptosis through ROSinduced cellular injury and activation of degenerative signaling cascades 20,21,22 .Mutual reinforcement between oxidative stress and inflammation establishes a pathological feedback loop that aggravates cartilage damage and joint deterioration 23,24 .In this study, OSR efficiently reduced intracellular ROS accumulation and enhanced intrinsic antioxidant defenses, thereby breaking this pathological feedback loop and improving cellular redox homeostasis

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The consistently higher HbA1C levels in the GLP-1 RAs group throughout the study suggesting the pleiotropic effects of GLP1RAs additional to glucose lowering effect 21

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