In vitro study demonstrates that berberine suppresses ferroptosis and promotes osteogenesis in high-glucose-exposed stem cells, indicating a protective mechanism via Nrf2/HO-1/GPX4 signaling.
To investigate the effects of BBR on ferroptosis and osteogenic differentiation in rat bone marrow mesenchymal stem cells (BMSCs) under high-glucose conditions and to explore the potential involvement of related molecular pathways. Rat BMSCs were isolated, cultured, and characterized in vitro. The optimal concentration of BBR was determined using the cell counting kit-8 assay. Intracellular ferroptosis markers were quantified using specific biochemical assay kits. The expression of ferroptosis-related genes and proteins was analyzed by real-time quantitative polymerase chain reaction and Western blotting. Osteogenic differentiation potential was assessed through alkaline phosphatase staining, alkaline phosphatase activity assay, alizarin red S staining, and RT-qPCR for osteogenesis-related genes. Cell migration capacity was evaluated by a scratch wound healing assay. The involvement of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4) signaling pathway was examined using RT-qPCR and Western blotting. High-glucose stimulation induced ferroptosis in rat BMSCs. BBR treatment dose-dependently inhibited ferroptosis while concurrently promoting osteogenic differentiation. The anti-ferroptotic and pro-osteogenic effects of BBR were found to be associated with changes in the Nrf2/HO-1/GPX4 signaling pathway and were partially reversed by co-treatment with a specific Nrf2 inhibitor. BBR inhibits ferroptosis and promotes osteogenic differentiation, effects that are associated with the Nrf2/HO-1/GPX4 signaling pathway.
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Chen et al. (2026) studied this question.
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