天然药物积雪草苷通过RANKL通路抑制破骨细胞分化,促进激素性股骨头坏死的修复

IF 0.7 4区 材料科学 Q3 Materials Science
Haijian Wu, Bowen Guo, Hongfa Zhong, Hui Ying
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引用次数: 0

摘要

积雪草苷是最经典的中药之一。核因子κ B受体激活因子(Receptor activator of nuclear factor - κ B Ligand, RANK)与核因子κ B受体激活因子(Receptor activator of nuclear factor - κ B)之间的相互作用激活了一系列细胞内信号通路。我们的研究探讨了积雪草苷通过RANKL途径抑制破骨细胞分化和激素性股骨头坏死(SIONFH)修复的机制。采用微针治疗系统(MTS)法检测积雪草苷对破骨细胞的影响,定量分析酒石酸盐耐酸性磷酸酶(TRAcP)多核细胞(3核)数量。通过羟基磷灰石包被板侵蚀面积和TRAcP染色检测不同剂量下骨功能的变化,检测不同骨细胞形成和成骨分化的表达。积雪草总苷对RANKL诱导的破骨细胞功能有减弱作用。当积雪草苷浓度为10 μ mol/L时,破骨细胞形成调控基因(NFATc1和Acp5)和破骨细胞功能相关基因(AP-1和P65)在RANKL存在下显著下调。积雪草苷(10 μ mol/L)通过抑制RANKL介导的NF- κ B活化和ca2 +振荡,显著降低RANKL诱导的钙振荡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Natural drug asiaticoside inhibits osteoclast differentiation and promotes repair of steroid-induced osteonecrosis of femoral head via RANKL pathway
Asiaticoside is one of the most classic traditional Chinese medicines. The interaction between Receptor activator of nuclear factor κ B (RANK) and Receptor Activator of Nuclear Factor- κ B Ligand (RANKL) activates a series of intracellular signaling pathways. Our research explored the mechanism of asiaticoside inhibiting osteoclast differentiation and repair of steroid-induced osteonecrosis of femoral head (SIONFH) through RANKL pathway. Asiaticoside’s effect on osteoclasts was determined by Microneedle Therapy System (MTS) method, and the number of Tartrate resistant acid phosphatase (TRAcP) multinucleated cells (3 nuclei) was quantitatively analyzed. Under different dose treatments, the changes of bone function were detected by eroded area and TRAcP staining on hydroxyapatite-coated plate, and the expression of different osteocyte formation and osteogenic differentiation were detected. Asiaticoside weakened the osteoclast function induced by RANKL. When the concentration of asiaticoside was 10 μ mol/L, osteoclast formation regulatory genes (NFATc1 and Acp5) and osteoclast cell function-related genes (AP-1 and P65) were significantly downregulated in the presence of RANKL. Asiaticoside (10 μ mol/L) significantly decreased calcium oscillations induced by RANKL via preventing RANKL-mediated NF- κ B activation and Ca 2+ oscillation.
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来源期刊
Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
0.00%
发文量
69
审稿时长
>12 weeks
期刊介绍: Information not localized
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