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<p>Rheumatoid arthritis (RA) is characterized by chronic synovitis, leading to joint cartilage and bone erosion. While current treatments aim to control inflammation, no specific drug prevents joint structure damage. This study set out to explore the efficacy of (5R)-5-hydroxytriptolide (LLDT-8), which targets osteoclasts known to be closely related to RA-induced erosion. We evaluated morphological changes of bone marrow cells and identified the induced osteoclasts by TRAP staining. LLDT-8’s inhibitory effect on the bone erosion activity of osteoclasts was assessed by resorption pit assay and the induction of apoptosis was evaluated by flow cytometry. Immunohistochemical staining was performed to detect the vascular endothelial growth factor (VEGF) expression in osteoclasts. LLDT-8 inhibited the transformation of bone marrow cells into osteoclast cells and induced the apoptosis of osteoclasts. Moreover, the number of osteoclasts-induced bone lacunae and the expression of VEGF expressions of osteoclasts were significantly reduced by LLDT-8. We demonstrated the critical function and mechanisms of LLDT-8 in osteoclast inhibition, providing new ideas for the potential effectiveness of intervention RA with LLDT-8.</p>

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Effects of (5R)-5-Hydroxytriptolide Against Rheumatoid Arthritis: Intervention on the Transformation of Bone Marrow Cells Induced Osteoclasts Bone Erosion and Angiogenesis

  • 期刊论文

  • 发表日期：

    2026年1月20日

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  • Ya Yan,
  • Hong Nie,
  • Yanling Lian,
  • Yi Shen,
  • Qin Ding

摘要

Rheumatoid arthritis (RA) is characterized by chronic synovitis, leading to joint cartilage and bone erosion. While current treatments aim to control inflammation, no specific drug prevents joint structure damage. This study set out to explore the efficacy of (5R)-5-hydroxytriptolide (LLDT-8), which targets osteoclasts known to be closely related to RA-induced erosion. We evaluated morphological changes of bone marrow cells and identified the induced osteoclasts by TRAP staining. LLDT-8’s inhibitory effect on the bone erosion activity of osteoclasts was assessed by resorption pit assay and the induction of apoptosis was evaluated by flow cytometry. Immunohistochemical staining was performed to detect the vascular endothelial growth factor (VEGF) expression in osteoclasts. LLDT-8 inhibited the transformation of bone marrow cells into osteoclast cells and induced the apoptosis of osteoclasts. Moreover, the number of osteoclasts-induced bone lacunae and the expression of VEGF expressions of osteoclasts were significantly reduced by LLDT-8. We demonstrated the critical function and mechanisms of LLDT-8 in osteoclast inhibition, providing new ideas for the potential effectiveness of intervention RA with LLDT-8.