〔Abstract〕 Objective To evaluate the anti-inflammatory activity of the novel magnolol ester derivative YW and to investigate its effects on chondrocyte senescence and preliminary mechanisms. Methods Magnolol and p-methylbenzoic acid were used as raw materials to synthesize the magnolol ester derivative YW (Molecular Formula: C26H24O3, Molecular Weight: 384.17, HPLC Purity >96%) via DCC/DMAP-catalyzed esterification. Cytotoxicity was assessed using the CCK-8 assay. A lipopolysaccharide (LPS)-induced RAW264.7 macrophage activation model and an interleukin-1β (IL-1β)-induced rat primary chondrocyte model were established. The release and mRNA expression of inflammatory factors including nitric oxide (NO), IL-1β, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay (ELISA), Griess reagent method, and quantitative real-time PCR (RT-qPCR). The expression of senescence markers such as inducible nitric oxide synthase (iNOS), pro-interleukin-1β (pro-IL-1β), lysine acetyltransferase 7 (KAT7), cyclin-dependent kinase inhibitor 1A (p21), and cyclin-dependent kinase inhibitor 2A (p16), as well as proteins related to chondrocyte extracellular matrix synthesis and catabolism, were analyzed by Western blot (WB). Molecular docking was performed using Discovery Studio 2019 to validate target binding. Results YW exhibited no significant cytotoxicity at concentrations ≤ 20μmol/L. YW concentration-dependently inhibited LPS-induced macrophage inflammatory cytokine release, significantly downregulated iNOS, Pro-IL-1β protein, and inflammatory cytokine mRNA expression (P<0.01). YW stably bound to KAT7 protein (binding energy: _94.2 kcal/mol); YW downregulated KAT7 and aging marker protein expression in naturally aged and IL-1β-induced chondrocyte models (P<0.01); YW regulated chondrocyte matrix synthesis and catabolic protein expression in IL-1β-induced chondrocytes (P<0.01). Conclusion YW inhibits macrophage activation and inflammatory cytokine release while downregulating KAT7 and senescence marker protein expression in chondrocytes, thereby blocking chondrocyte senescence.