​Sarcopenia is an age-related condition causing skeletal muscle loss and weakness, increasing risks of hospitalization, fractures, and mortality. Excess glucocorticoids (GCs) from aging or medication accelerate muscle breakdown and inhibit synthesis, worsening sarcopenia. However, no approved drug treatments exist, highlighting the need for alternatives. This study examined postbiotics in a sarcopenia model using C2C12 myotubes (in vitro) and SD rats (in vivo). Postbiotics, bioactive compounds from non-viable microorganisms, have anti-inflammatory and antioxidant effects. Here, we tested their potential to protect against dexamethasone (DEX)-induced muscle protein degradation. In vitro, C2C12 myoblasts were differentiated for four days, pretreated with postbiotics for 48 hours, and exposed to 100 μM DEX for 24 hours. Postbiotics showed no cytotoxicity up to 200 μg/mL (48 h). They reduced DEX-induced morphological changes in a dose-dependent manner and inhibited key proteins in the ubiquitin-proteasome system (UPS), a major muscle protein degradation pathway. In vivo, DEX reduced muscle mass and strength, but postbiotics preserved both in a dose-dependent manner. They also suppressed MuRF1 and MAFbx/atrogin-1, key regulators of muscle protein degradation. These findings suggest postbiotics may counteract DEX-induced muscle loss and serve as a functional food ingredient for sarcopenia management.