Combination of 20(R)-Rg3 and HUCMSCs Alleviates Type 2 Diabetes Mellitus in C57BL/6 Mice by Activating the PI3K/Akt Signaling Pathway
Summary: T2DM mouse model induced by high-fat diet (HFD) and streptozotocin (STZ) in C57BL/6 mice; interventions include HUCMSCs (human umbilical cord mesenchymal stem cells) combined with 20(R)-Rg3 treatment. Combination therapy improved insulin sensitivity (reduced HOMA-IR, enhanced OGTT/IPITT), lowered blood glucose, promoted pancreatic islet regeneration, reduced apoptosis, decreased inflammatory markers (TNF-α, IL-1β), and activated PI3K/Akt pathway via upregulated genes in transcriptomic analysis. The diabetic foot ulcer (DFU) is not merely a passive sequel to chronic hyperglycemia but functions as an active inflammatory focus. Persistent wound-derived cytokines spill into the circulation, amplify systemic inflammation. Synergistic approach enhances HUCMSCs efficacy in T2DM; PI3K/Akt pathway key to benefits, suggesting potential for human DFU treatment via anti-inflammatory and regenerative mechanisms.
Key Highlights:
- Methods: HFD/STZ-induced T2DM mice; 20(R)-Rg3 pretreated HUCMSCs via tail vein.
- Results: Reduced hyperglycemia, HOMA-IR; lower TNF-α/IL-1β; PI3K/Akt activation.
- DFU Link: Ulcers as inflammatory hubs amplifying systemic effects.
- Implications: Targets for wound healing in diabetic complications.
- Authors: Zhou Z, Zheng J, Guo X et al.
Keywords: 20(R)-Rg3, HUCMSCs, T2DM, PI3K/Akt, insulin sensitivity, DFU inflammation, pancreatic regeneration