Extract of Aerial Parts of "Tongchaeru" Sweet Potato Attenuates Muscle Atrophy via Mitochondrial Improvement and PI3K-Akt Pathway Activation in a Mouse Model.

Abstract

Skeletal muscle atrophy triggered by glucocorticoid is linked to impaired mitochondrial function and dysregulated protein metabolism. While the metabolic benefits of sweet potato roots have been widely studied, the anti-atrophic potential of their edible aerial parts on the muscle remains unexplored. This study examined the protective role of an aqueous extract of Tongchaeru aerial parts (TE), a sweet potato cultivar newly developed in Korea. The major phenolic compounds in TE were estimated using UPLC. Male mice were received dexamethasone (Dex, 10 mg/kg body weight) to trigger muscle atrophy and co-treated orally with TE at doses of 200 or 400 mg/kg for 14 days. Grip strength (GS), muscle histology, markers of mitochondrial biogenesis and respiratory complexes, and protein metabolic signaling pathways were evaluated. TE significantly improved GS and increased the cross-sectional area of the quadriceps and gastrocnemius muscles. TE reversed Dex-mediated downregulation of mitochondrial biogenesis-associated biomolecules (PGC-1α, NRF1, and TFAM) and restored the expression of oxidative phosphorylation (OXPHOS) components. TE attenuated AMPK-FoxO3α activation and reduced the expression of muscle degradation-related factors, including atrogin-1, MuRF1, and myostatin, while counteracting Dex-induced suppression of the PI3K-Akt-mTOR signaling pathway and muscle protein synthesis markers (MyoD1, MyoG, and MHC). Phenolic profiling revealed that TE contains high levels of neochlorogenic acid, chlorogenic acid, and caffeic acid. These findings suggest that TE mitigates Dex-induced skeletal muscle atrophy by restoring mitochondrial function, reducing protein degradation, and maintaining protein synthesis. TE may act as a nutraceutical with preventive effects on muscle wasting.