Abstract
Magnesium lithospermate B (MLB) is a primary hydrophilic component of Danshen, the dried root of Salvia miltiorrhiza used in traditional medicine, and its beneficial effects on obesity-associated metabolic abnormalities were reported in our previous study. The present study investigated the anti-muscle atrophy potential of MLB in mice with high-fat diet (HFD)-induced obesity. In addition to metabolic abnormalities, the HFD mice had a net loss of skeletal muscle weight and muscle fibers and high levels of muscle-specific ubiquitin E3 ligases, namely the muscle atrophy F-box (MAFbx) and muscle RING finger protein 1 (MuRF-1). MLB supplementation alleviated those health concerns. Parallel changes were revealed in high circulating tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), skeletal TNF receptor I (TNFRI), nuclear factor-kappa light chain enhancer of activated B cells (NF-κB), p65 phosphorylation, and Forkhead box protein O1 (FoxO1) as well as low skeletal phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt) phosphorylation. The study revealed that MLB prevented obesity-associated skeletal muscle atrophy, likely through the inhibition of MAFbx/MuRF-1-mediated muscular degradation. The activation of the PI3K-Akt-FoxO1 pathway and inhibition of the TNF-α/TNFRI/NF-κB pathway were assumed to be beneficial effects of MLB.
Highlights
Muscle atrophy occurs as a result of a net loss of muscle mass
These results suggested that Magnesium lithospermate B (MLB) supplementation alleviated high-fat diet (HFD)-induced adiposity
This study demonstrated that MLB supplementation attenuated obesity-associated skeletal muscle atrophy in HFD mice through the regulation of the phosphoinositide 3-kinase (PI3K)/Akt/Forkhead box protein O1 (FoxO1) and tumor necrosis factor-α (TNF-α)/NF-κB signaling pathways, leading to the inhibition of muscle-specific ubiquitin E3 ligase expression
Summary
Muscle atrophy occurs as a result of a net loss of muscle mass. In addition to its devastating effects on human health, muscle atrophy is a highly recognized risk factor for physical disabilities and a poor quality of life [1,2]. The majority of muscle mass depends on the counterbalance between protein anabolism and catabolism. Insufficient protein synthesis and overwhelmed protein degradation predispose people to muscle atrophy [3,4]. The prevalence of muscle atrophy is continually increasing because it is a complication of many acute and chronic diseases [5]. A more comprehensive understanding of its pathogenic mechanism is necessary for the development of strategies to combat it and its associated sequelae
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