摘要
Glucocorticoid-associated skeletal muscle wasting poses a significant clinical issue,stemming from a dysregulation between the synthesis and breakdown of muscle protein.To investigate potential countermeasures,we examined the effects of an amino acid-epigallocatechin gallate mixture(AA-EGCG),composed of cysteine,glutamine,leucine,and EGCG,in dexamethasone(DEX)-treated C2C12 myotubes and C57BL/6 mice.DEX administration induced pronounced muscle atrophy,with reduced myotube size,suppressed expression of myogenic and anabolic markers(MyoD1,myogenin,PI3K/Akt/mTOR),and activation of catabolic mediators(FoxO3a,MuRF1,Atrogin-1).Mitochondrial biogenesis and antioxidant signaling were also impaired via downregulation of the SIRT1-PGC1αaxis.The AA-EGCG effectively mitigated DEX-triggered muscle atrophy,showing a concentration-dependent effect.It preserved myotube morphology,enhanced myogenic differentiation,restored PI3K/Akt/mTOR signaling,and suppressed FoxO3a-mediated proteolysis.Moreover,it upregulated SIRT1,PGC-1α,and related regulators,thereby enhancing mitochondrial function and defense against oxidative.In vivo,AA-EGCG further prevented muscle mass loss,normalized serum biomarkers,and improved physical performance in DEX-treated mice.Collectively,these findings identify AA-EGCG as a multi-targeted nutritional strategy that mitigates glucocorticoid-induced muscle wasting by coordinating anabolic,catabolic,and mitochondrial pathways.
基金
supported by BioLAB Co.Ltd(Guri-si,Republic of Korea)。
