Astragalus Polysaccharide Activates the AKT-mTOR Pathway to Reduce ROS and Promote Intramuscular Protein Levels in Sarcopenia Mice

Background Astragalus polysaccharide (APS), a component of traditional Chinese medicine, has recently shown promise in treating sarcopenia. Purpose This study investigates APS’s potential to reduce reactive oxygen species (ROS) and promote intramuscular protein levels in sarcopenic mice by activating the AKT-mammalian target of rapamycin (mTOR) pathway. Materials and Methods By constructing a mouse model of sarcopenia and dividing it into a blank model group, a low, medium and high concentration group, a model group as well as a control group, the therapeutic effect and mechanism of Astragali polysaccharides on sarcopenia were observed through animal experiments, obtaining gastrocnemius muscle to carry out in vitro cellular experiments, respectively and polymerase chain reaction (PCR), Sirius staining, immunofluorescence microscopy, Western blot (WB) experiments, and so on, combined with the simulation of the oxidative environment of ROS in vitro , to observe the level of AKT-mammalian target of rapamycin (mTOR) markers, superoxide dismutase 2 (Sod2) gene level and level of each protein in mouse muscle cells. Results (a) The animal model of myasthenia gravis was successfully established. (b) The effect of APS in the treatment of myasthenia gravis was outstanding and concentration dependent. (c) Compared with the model group, AKT was upregulated in the Astragali polysaccharide group, the proliferation rate of muscle cells was increased, and Sod2 messenger ribonucleic acid (mRNA) was elevated, while ROS was reduced. (d) Compared with the Astragali polysaccharide group, AKT was upregulated in + SC79 group, while muscle cell proliferation rate increased, Sod2 mRNA expression was significantly elevated, and ROS content was reduced. (e) Sod2 mRNA and matrix metallopeptidase 1 (MMP-1) protein expression in the Astragali polysaccharide + N -acetylcysteine (NAC) group were significantly higher, while ROS, collagen-1, and TIMP metallopeptidase inhibitor 1 (TIMP-1) levels were lower. (f) Compared with Astragali polysaccharide + SC79 group, collagen-1, TIMP-1, p38 mitogen-activated protein kinase (p38MAPK) protein expression in cells of Astragali polysaccharide + SC79 + NAC group was significantly reduced, while MMP-1 content was elevated. (g) Compared with the Astragali polysaccharide + SC79 + NAC group, cellular collagen-1, TIMP-1, and p38MAPK were elevated, and MMP-1 content was decreased in the Astragali polysaccharide + SC79 + NAC + hydrogen peroxide group. Conclusion APS treatment improves muscle cell proliferation and enhances sarcopenia mice’s anti-oxidant capacity by activating phosphoinositide 3-kinase (PI3K)/AKT to inhibit ROS, effectively maintaining the intracellular redox balance.