Role Of Gpx6 In TMJ OA Cartilage Damage

This study explores GPx6′s function in TMJ OA and its therapeutic potential. This study was approved by the Medical Ethics Committee. A TMJ OA SD rat model (Newly weaned male SD rats at 3 weeks of age) was established. RT-qPCR and Western blotting were used to detect GPx6 mRNA and protein expression levels in TMJ cartilage. Safranin O-Fast Green staining was performed to assess proteoglycan expression, while immunohistochemistry was used to evaluate ECM molecules (Aggrecan, ACAN), degradative enzymes (MMP13 and ADAMTS5), and chondrocyte differentiation markers (RUNX2 and COL10). An IL-1β-induced rat condylar chondrocyte injury model were constructed to examine GPx6 expression, ECM components, degradative enzymes, and chondrocyte differentiation markers. The GPx6 recombinant plasmid was transfected into IL-1β-induced rat condylar chondrocytes to assess the effects of GPx6 overexpression on oxidative damage markers (MDA, ROS) and antioxidant enzymes (SOD, GSH/GSSG ratio). 1. GPx6 was downregulated in TMJ OA, with ECM degradation (ACAN↓, MMP13↑) and abnormal hypertrophy (RUNX2/COL10). 2. GPx6 overexpression reduced oxidative damage and partially restored ECM and differentiation. GPx6 deficiency exacerbates TMJ OA cartilage damage. GPx6 upregulation may be a therapeutic strategy.