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<p>In chronic inflammatory microenvironments, TNF-α disrupts bone remodeling by suppressing osteogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs), while conventional TNF-α inhibitors lack osteoprotective effects. This study reveals that naringenin counteracts TNF-α-induced osteogenic suppression by potentially targeting AKR1B1 to restore redox balance and inhibit NF-κB-mediated inflammation. In vitro experiments demonstrated that naringenin restored osteogenic capacity in TNF-α-treated hBMSCs, enhancing ALP activity, mineralization, and expression of RUNX2/OCN while reducing IL-6/IL-1β levels. Mechanistically, naringenin scavenged free radicals, elevated SOD/CAT activity, and attenuated TNF-α-driven ROS accumulation. Bioinformatics analysis identified TNF-α-activated NF-κB signaling and upregulation of the oxidative stress enzyme AKR1B1, with molecular docking confirming strong binding between naringenin and AKR1B1. This study pioneers AKR1B1 as a novel therapeutic target for inflammatory bone loss, demonstrating naringenin’s synergistic “antioxidant-anti-inflammatory-pro-osteogenic” effects. These findings provide a theoretical foundation for phytochemical applications in orthopedic therapies and highlight potential clinical translation strategies.</p>

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Naringenin restores osteogenic differentiation in TNF-α-Treated bone marrow mesenchymal stem cells by targeting AKR1B1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月31日

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  • Bin He,
  • Feng He,
  • Huimin Li,
  • Leyi Huang

摘要

In chronic inflammatory microenvironments, TNF-α disrupts bone remodeling by suppressing osteogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs), while conventional TNF-α inhibitors lack osteoprotective effects. This study reveals that naringenin counteracts TNF-α-induced osteogenic suppression by potentially targeting AKR1B1 to restore redox balance and inhibit NF-κB-mediated inflammation. In vitro experiments demonstrated that naringenin restored osteogenic capacity in TNF-α-treated hBMSCs, enhancing ALP activity, mineralization, and expression of RUNX2/OCN while reducing IL-6/IL-1β levels. Mechanistically, naringenin scavenged free radicals, elevated SOD/CAT activity, and attenuated TNF-α-driven ROS accumulation. Bioinformatics analysis identified TNF-α-activated NF-κB signaling and upregulation of the oxidative stress enzyme AKR1B1, with molecular docking confirming strong binding between naringenin and AKR1B1. This study pioneers AKR1B1 as a novel therapeutic target for inflammatory bone loss, demonstrating naringenin’s synergistic “antioxidant-anti-inflammatory-pro-osteogenic” effects. These findings provide a theoretical foundation for phytochemical applications in orthopedic therapies and highlight potential clinical translation strategies.