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| 肉豆蔻酸延缓黄韧带成纤维细胞/骨髓间充质干细胞衰老调控成骨的机制 |
| Myristic acid delaying ligamentum flavum cell/bone marrow mesenchymal stem cellsenescence and regulating osteogenesis based on the theory of "Treating Different Diseases with the Same Method" |
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| DOI：10.3969/j.issn.1006-7108.2025.10.002 |
| 中文关键词: 肉豆蔻酸 黄韧带骨化症 老年性骨质疏松 异病同治 |
| 英文关键词:myristic acid ligamentum flavum ossification senile osteoporosis the theory of "treating different diseases with the same method" |
| 基金项目:国家自然科学基金( 882205230，82274542，82274615，82205137)；广东省中医药局项目（20221131） |
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| 中文摘要: |
| 目的 探讨肉豆蔻酸通过延缓黄韧带成纤维细胞与骨髓间充质干细胞衰老调控成骨的机制。方法 临床研究中回顾性分析相关数据，探讨黄韧带骨化症与骨密度的相关性；体外实验中观察黄韧带骨化过程中组织形态学变化，同时检测肉豆蔻酸对衰老的黄韧带成纤维细胞和骨髓间充质干细胞成骨能力的影响。结果 临床研究中发现L1-L4椎体骨密度、股骨颈骨密度、髋关节骨密度和黄韧带CT值均显著高于正常组（P＜0.001），并且黄韧带骨化程度与髋关节（R=0.451，P＜0.001）、L1-L4椎体（R=0.412，P＜0.001）、股骨颈（R=0.451，P＜0.001）骨密度呈显著正相关；体外实验提示黄韧带在骨化过程中出现弹性纤维/胶原纤维比例失衡和巨噬细胞及衰老蛋白的富集；此外，黄韧带成纤维细胞和骨髓间充质干细胞在衰老过程中成骨能力呈现相反的趋势（前者增强，后者减弱），而肉豆蔻酸能够延缓两种细胞的衰老，并使两者的成骨能力分别减弱和增强。结论 黄韧带骨化人群的骨密度显著高于正常人群，且与骨化程度呈线性关系，肉豆蔻酸可延缓黄韧带成纤维细胞衰老并减少其病理性成骨，延缓骨髓间充质干细胞衰老并增强其成骨能力，具有防治黄韧带骨化症和老年性骨质疏松的潜力。 |
| 英文摘要: |
| Objective Investigating the mechanism of myristic acid (MA) regulates osteogenesis by delaying senescence of ligamentum flavum cells (LFC) and bone marrow mesenchymal stem cells (BMSCs). Methods The correlation between ligamentum flavum ossification (OLF) and bone mineral density (BMD) was investigated in a retrospective clinical study. The changes of morphology during the process of OLF were observed and the effect of MA on the osteogenic capacity by delaying senescence ofLFC and BMSCs was detected in in vitro experiments. Results The BMD of L1-L4 vertebral body, femoral neck, hip joint, and the CT value of ligamentum flavum in patients with OLF were significantly higher(P<0.001). The degree of OLF was significantly positively correlated with the BMD of the hip joint (R=0.451, P<0.001), L1-L4 vertebral body (R=0.412, P<0.001), and femoral neck (R=0.451, P<0.001) in correlation analysis. Pathological staining suggests an imbalance in the ratio of elastic fibers/collagen fibers and enrichment of macrophages and aging proteins in the process of OLF. In addition, we also found that the osteogenic ability of LFC and BMSCs showed an opposite trend during the aging process, the former increases, the latter decreases, and MA can delay the aging of both types of cells, while weakening the former and enhancing the latter's osteogenic ability. Conclusion The BMD of individuals with OLF is significantly higher than normal population, and it is linearly related to the degree of ossification. MA can delay the senescence of LFC and reduce their pathological osteogenesis, delay the senescence of BMSCs and enhance their osteogenic capacity, with the potential to prevent OLF and senile osteoporosis (SOP). |
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