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Ginsenoside Rb1 regulates CPT1A deacetylation to inhibit intramuscular fat infiltration after rotator cuff tear
Yuesong Yin1, Zili Wang1, Yian Yang2
1Department of Orthopaedics, The Third Xiangya Hospital, Central South University, No. 138 Tongzipo Road, Changsha 410013, China.
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 6 weeks 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.
Insights
Ginsenoside Rb1 reduces fat infiltration in rotator cuff muscles after tears. This compound activates SIRT1, promoting fatty acid breakdown and potentially improving rotator cuff repair outcomes.
Area of Science:
- Muscle regeneration and molecular biology
- Biochemistry and metabolic pathways
- Orthopedic research
Background:
- Fat infiltration (FI) in rotator cuff muscles correlates with poor outcomes and failed repairs of rotator cuff tears (RCTs).
- Understanding molecular mechanisms to inhibit FI is crucial for improving RCT treatment.
- Ginsenosides are being explored for therapeutic potential in various conditions.
Purpose of the Study:
- To investigate the role of ginsenoside Rb1 in inhibiting muscle fat infiltration after rotator cuff injury.
- To elucidate the underlying molecular mechanism of Rb1's action in this context.
Main Methods:
- A tendinous transfer (TT) model was used in mice to simulate rotator cuff tears.
- Mice were treated with ginsenoside Rb1 or other ginsenoside components for 6 weeks.
- Molecular analysis focused on Rb1's interaction with SIRT1 and its downstream effects on CPT1A and fatty acid metabolism.
Main Results:
- Rb1 treatment significantly reduced fat infiltration in the supraspinatus (SS) muscle compared to control groups.
- Rb1 was found to bind to the NAD+ domain of SIRT1, increasing its expression and enzymatic activity.
- Rb1-mediated SIRT1 activation led to deacetylation of CPT1A, enhancing fatty acid beta-oxidation and lipolysis in adipocytes.
Conclusions:
- Ginsenoside Rb1 effectively inhibits fat infiltration in rotator cuff muscles post-injury.
- The mechanism involves the activation of SIRT1, which promotes fatty acid metabolism.
- Rb1 shows promise as a therapeutic agent for improving outcomes in patients with rotator cuff tears.
