Heat-Treated Lactiplantibacillus plantarum KM2 Fermentation Ameliorate Muscular Atrophy
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Sarcopenia, a progressive loss of skeletal muscle mass and function, poses a significant health concern in aging populations and cancer patients. Despite ongoing pharmaceutical research, including drug repurposing strategies, no FDA-approved treatment is currently available for sarcopenia, highlighting the need for safer, food-derived interventions. This study evaluated the anti-aging and muscle-preserving effects of KLP_KM2, a postbiotic formulation derived from Lactiplantibacillus plantarum KM2, using Caenorhabditis elegans and C2C12 muscle cell models. In C. elegans, KLP_KM2 and its components significantly extended lifespan, reduced lipofuscin accumulation, enhanced pharyngeal pumping, and preserved coordinated movement patterns. These effects were accompanied by upregulation of longevity, immune/stress response, and muscle function-related genes. In C2C12 myotubes, KLP_KM2 treatment mitigated CT26-conditioned medium-induced muscle atrophy, restoring myotube diameter and length, increasing expression of myogenic markers (MyoD, myogenin, MHC I, MHC IIa), and downregulating atrophy markers (Atrogin-1, MuRF1). These findings suggest that KLP_KM2 may serve as a promising postbiotic intervention to support muscle health, prevent sarcopenia, and counteract cancer cachexia. Further in vivo mammalian studies and clinical trials are warranted to validate its therapeutic potential.
Abstract
Sarcopenia, a progressive loss of skeletal muscle mass and function, poses a significant health concern in aging populations and cancer patients. Despite ongoing pharmaceutical research, including drug repurposing strategies, no FDA-approved treatment is currently available for sarcopenia, highlighting the need for safer, food-derived interventions. This study evaluated the anti-aging and muscle-preserving effects of KLP_KM2, a postbiotic formulation derived from Lactiplantibacillus plantarum KM2, using Caenorhabditis elegans and C2C12 muscle cell models. In C. elegans, KLP_KM2 and its components significantly extended lifespan, reduced lipofuscin accumulation, enhanced pharyngeal pumping, and preserved coordinated movement patterns. These effects were accompanied by upregulation of longevity, immune/stress response, and muscle function-related genes. In C2C12 myotubes, KLP_KM2 treatment mitigated CT26-conditioned medium-induced muscle atrophy, restoring myotube diameter and length, increasing expression of myogenic markers (MyoD, myogenin, MHC I, MHC IIa), and downregulating atrophy markers (Atrogin-1, MuRF1). These findings suggest that KLP_KM2 may serve as a promising postbiotic intervention to support muscle health, prevent sarcopenia, and counteract cancer cachexia. Further in vivo mammalian studies and clinical trials are warranted to validate its therapeutic potential.