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<p>Postmenopausal osteoporosis (PMOP) is a skeletal disorder marked by progressive bone mineral density decline and increased susceptibility to fractures. Accumulating evidence indicates that coupled osteogenesis and angiogenesis are indispensable for bone remodeling and repair. This study investigated the therapeutic potential of dendrobine in concurrently modulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and angiogenic activity in the context of PMOP. BMSCs were isolated from Sprague-Dawley rats and rigorously characterized prior to experimentation. Cell viability was quantified using CCK-8 assays, and apoptosis was assessed via flow cytometry. To evaluate angiogenesis, tube formation capacity was measured following coculture of BMSCs and human umbilical vein endothelial cells (HUVECs), and protein levels of angiogenic factors (VEGF, MMP2, and MMP9) were quantified by western blotting. Osteogenic differentiation was assessed by Alizarin red staining for mineralized nodule formation, ALP staining, and western blotting of osteogenic markers (Runx2, OCN, and OPN). Following PMOP modeling via bilateral ovariectomy (OVX), H&amp;E staining and micro-computed tomography were conducted. Western blotting was performed to measure protein levels of core Hippo pathway components (Mst1, Lats1, Yap1, and Taz) in femoral bone tissue. Results showed that dendrobine significantly promoted BMSC viability and suppressed apoptosis in a dose-dependent manner. In BMSC-HUVEC cocultures, dendrobine markedly augmented tube formation and upregulated VEGF, MMP2, and MMP9. Concurrently, dendrobine enhanced osteogenic differentiation, as evidenced by increased ALP activity, enhanced mineralization, and elevated protein levels of Runx2, OCN, and OPN. In OVX rats, dendrobine treatment ameliorated trabecular bone loss and restored bone parameters toward sham levels. Consistently, dendrobine elevated the expression of osteogenic and angiogenic proteins in vivo. Moreover, dendrobine suppressed Mst1 and Lats1 expression while promoting Yap1 and Taz expression in OVX rats. In conclusion, dendrobine alleviates PMOP by coordinately enhancing osteogenesis and angiogenesis through inhibition of the Hippo pathway and subsequent activation of the Yap1/Taz signaling.</p>

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Dendrobine promotes osteogenesis-angiogenesis in postmenopausal osteoporosis by inhibiting Hippo signaling pathway

  • 期刊论文

  • 发表日期：

    2026年5月13日

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  • Xiangping Meng,
  • Xingtao Chen,
  • Jin Huang

摘要

Postmenopausal osteoporosis (PMOP) is a skeletal disorder marked by progressive bone mineral density decline and increased susceptibility to fractures. Accumulating evidence indicates that coupled osteogenesis and angiogenesis are indispensable for bone remodeling and repair. This study investigated the therapeutic potential of dendrobine in concurrently modulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and angiogenic activity in the context of PMOP. BMSCs were isolated from Sprague-Dawley rats and rigorously characterized prior to experimentation. Cell viability was quantified using CCK-8 assays, and apoptosis was assessed via flow cytometry. To evaluate angiogenesis, tube formation capacity was measured following coculture of BMSCs and human umbilical vein endothelial cells (HUVECs), and protein levels of angiogenic factors (VEGF, MMP2, and MMP9) were quantified by western blotting. Osteogenic differentiation was assessed by Alizarin red staining for mineralized nodule formation, ALP staining, and western blotting of osteogenic markers (Runx2, OCN, and OPN). Following PMOP modeling via bilateral ovariectomy (OVX), H&E staining and micro-computed tomography were conducted. Western blotting was performed to measure protein levels of core Hippo pathway components (Mst1, Lats1, Yap1, and Taz) in femoral bone tissue. Results showed that dendrobine significantly promoted BMSC viability and suppressed apoptosis in a dose-dependent manner. In BMSC-HUVEC cocultures, dendrobine markedly augmented tube formation and upregulated VEGF, MMP2, and MMP9. Concurrently, dendrobine enhanced osteogenic differentiation, as evidenced by increased ALP activity, enhanced mineralization, and elevated protein levels of Runx2, OCN, and OPN. In OVX rats, dendrobine treatment ameliorated trabecular bone loss and restored bone parameters toward sham levels. Consistently, dendrobine elevated the expression of osteogenic and angiogenic proteins in vivo. Moreover, dendrobine suppressed Mst1 and Lats1 expression while promoting Yap1 and Taz expression in OVX rats. In conclusion, dendrobine alleviates PMOP by coordinately enhancing osteogenesis and angiogenesis through inhibition of the Hippo pathway and subsequent activation of the Yap1/Taz signaling.