Abstract
Fat infiltration (FI) in the rotator cuff muscle is associated with poor clinical outcomes and failed repair of rotator cuff tears (RCTs) in patients. In this study, we aimed to investigate the function of ginsenoside Rb1 in inhibiting FI in muscles after RCT and its underlying molecular mechanism. After TT modeling, mice treated with Rb1 for 6weeks showed lower FI in the SS muscle compared with mice in the control groups and those treated with other ginsenoside components. Mechanically, Rb1 binds to the NAD+ domain of SIRT1, activating its expression and enzyme activity. This activation stimulates the deacetylation of CPT1A at site K195, thereby promoting fatty acid β-oxidation in adipocyte cells and improving lipolysis. These findings suggest that Rb1 is a potential therapeutic component for improving the outcomes of patients with RCTs.
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