Standardized Boesenbergia pandurata Extract Prevents Dexamethasone-Induced Muscle Atrophy and Dysfunction in C57BL/6 Mice

Abstract

Muscle atrophy, characterized by diminished muscle mass and impaired function, poses a substantial global health concern. Boesenbergia pandurata (Roxb.) Schltr., commonly known as fingerroot, possesses a variety of advantageous activities, including anti-inflammatory, antioxidant, antibacterial, and anticancer effects. However, there are currently no preclinical studies available that explore the potential of B. pandurata extract (BPE) to mitigate muscle atrophy. In this study, we aimed to explore the protective effects of BPE, standardized to panduratin A content, against muscle atrophy and its underlying molecular mechanisms in a dexamethasone-induced muscle atrophy mouse model. Compared with the dexamethasone group, BPE significantly restored muscle mass, muscle volume, muscle fiber cross-sectional area, grip strength, and exercise endurance. Additionally, BPE suppressed inflammatory responses by downregulating the expressions of nuclear factor kappa B and inflammatory cytokines while also enhancing antioxidant effects by increasing the expressions of antioxidant enzymes. Moreover, BPE promoted protein synthesis and muscle differentiation by stimulating the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling pathway. Furthermore, it suppressed myostatin expression and inhibited the expressions of E3 ubiquitin ligases by preventing the nuclear translocation of forkhead box O3a, thereby alleviating proteolysis. Overall, BPE effectively regulates unbalanced protein metabolism, suggesting its potential as a functional food ingredient for preventing muscle wasting diseases.