Antioxidant Activity of Protects against Dexamethasone-Induced Muscle Atrophy.

Skeletal muscle atrophy is defined as wasting or loss of muscle. Although glucocorticoids (GCs) are well-known anti-inflammatory drugs, their long-term or high-dose use induces skeletal muscle atrophy. (VF) is used to treat restlessness, anxiety, and sleep disorders; however, its effects on skeletal muscle health have not been investigated. This study investigated whether could ameliorate muscle atrophy. We induced muscle atrophy and , by treatment with dexamethasone (DEX), a synthetic GC. In DEX-induced myotube atrophy, treatment increased the fusion index and decreased the expression of muscle atrophic genes such as muscle atrophy F-box (MAFbx/Atrogin-1) and muscle RING-finger protein 1 (MuRF1). In DEX-treated mice with muscle atrophy, supplementation increased the ability to exercise, muscle weight, and cross-sectional area, whereas it inhibited myosin heavy chain isoform transition and the expression of muscle atrophy biomarkers. treatment led to via the downregulation of muscle atrophic genes via inhibition of GC receptor translocation. was also found to act as a reactive oxygen species (ROS) scavenger. Didrovaltrate (DI), an iridoid compound from , was found to downregulate atrophic genes and decrease ROS in the DEX-induced myotube atrophy. Consolidated, our results indicate that prevents DEX-induced muscle atrophy by inhibiting GC receptor translocation. Further, acts as a ROS scavenger, and its functional compound is didrovaltrate. We suggest that and its functional compound didrovaltrate possess therapeutic potentials against muscle atrophy.