Abstract
Low-intensity pulsed ultrasound (LIPUS) has been proved to promote the proliferation of myoblast C2C12. However, whether LIPUS can effectively prevent muscle atrophy has not been clarified, and if so, what is the possible mechanism. The aim of this study is to evaluate the effects of LIPUS on muscle atrophy in hindlimb unloading rats, and explore the mechanisms. The rats were randomly divided into four groups: normal control group (NC), hindlimb unloading group (UL), hindlimb unloading plus 30 mW/cm2 LIPUS irradiation group (UL + 30 mW/cm2), hindlimb unloading plus 80 mW/cm2 LIPUS irradiation group (UL + 80 mW/cm2). The tails of rats in hindlimb unloading group were suspended for 28 days. The rats in the LIPUS treated group were simultaneously irradiated with LIPUS on gastrocnemius muscle in both lower legs at the sound intensity of 30 mW/cm2 or 80 mW/cm2 for 20 min/d for 28 days. C2C12 cells were exposed to LIPUS at 30 or 80 mW/cm2 for 5 days. The results showed that LIPUS significantly promoted the proliferation and differentiation of myoblast C2C12, and prevented the decrease of cross-sectional area of muscle fiber and gastrocnemius mass in hindlimb unloading rats. LIPUS also significantly down regulated the expression of MSTN and its receptors ActRIIB, and up-regulated the expression of Akt and mTOR in gastrocnemius muscle of hindlimb unloading rats. In addition, three metabolic pathways (phenylalanine, tyrosine and tryptophan biosynthesis; alanine, aspartate and glutamate metabolism; glycine, serine and threonine metabolism) were selected as important metabolic pathways for hindlimb unloading effect. However, LIPUS promoted the stability of alanine, aspartate and glutamate metabolism pathway. These results suggest that the key mechanism of LIPUS in preventing muscle atrophy induced by hindlimb unloading may be related to promoting protein synthesis through MSTN/Akt/mTOR signaling pathway and stabilizing alanine, aspartate and glutamate metabolism.
Highlights
Muscular atrophy is associated with metabolic abnormalities, including changes in insulin sensitivity, increased fat and connective tissue infiltration in skeletal muscle, decreased hormone levels, decreased mitochondrial activity, resulting in impaired oxidative defense, and severe bone loss resulting in osteoporosis [11,12]
Our previous studies have reported that Low-intensity pulsed ultrasound (LIPUS) significantly promoted exercise-induced muscle hypertrophy and prevented muscle atrophy caused by type 1 diabetes [14]
The results showed that LIPUS could significantly promote the proliferation of C2C12, which was consistent with the results of Imashiro et al [39]
Summary
In the long-term lack of mechanical stimulation, the size, strength, volume and crosssectional area of skeletal muscle will be significantly reduced. Muscular atrophy is associated with metabolic abnormalities, including changes in insulin sensitivity, increased fat and connective tissue infiltration in skeletal muscle, decreased hormone levels, decreased mitochondrial activity, resulting in impaired oxidative defense, and severe bone loss resulting in osteoporosis [11,12]. Our previous studies have reported that LIPUS significantly promoted exercise-induced muscle hypertrophy and prevented muscle atrophy caused by type 1 diabetes [14]. The effect of LIPUS on the metabonomics of muscle atrophy has not been reported. We investigate the effects of LIPUS on muscle atrophy in tail suspended rats, and analyze the underlying mechanism from the perspective of metabonomics. Myostatin (MSTN), a key negative regulator of muscle growth and development, which has strong catabolic and anti-anabolic effects on skeletal muscle were evaluated
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