Liu Xiangwei, Wang Binfeng
Department of Traumatic Orthopedics, Chifeng Municipal Hospital, Chifeng, Inner Mongolia, China.
Department of Traumatic Orthopedics, Chifeng Municipal Hospital, Chifeng, Inner Mongolia, China. Email:
Cell J. 2021 Sep;23(4):451-456. doi: 10.22074/cellj.2021.7736. Epub 2021 Aug 29.
This study evaluated the beneficial effect of fuscoside in the repair of bone defects (BDs) and the possible molecular mechanism thereof.
In this experimental study, a BD was induced by drilling the rat tibia. The rats were then administered oral fuscoside, at 200 or 300 mg/kg, for 2 weeks. The effect of treatment was assessed based on the bone formation score and on the levels of cytokines and biochemical markers in serum. Tibial expression of the proteins involved in the Rankl/Nlrp3/Opg pathway was determined by quantitative reverse-transcription polymerase chain reaction and western blot assay, and histopathological changes by haematoxylin and eosin and TRAP staining.
In the fuscoside-treated BD rats, the bone formation score improved and inflammatory cytokine levels were reduced. The levels of biochemical markers improved as well, as did the expression of apoptosis proteins. Fuscoside also attenuated the expression of Rankl, Opg, Nlrp3, Runx2, Osterix, and Osteocalcin (Oc) proteins in the tibial tissue of the BD rats and reversed the abnormal histopathological changes.
These results suggest that fuscoside improves BD repair by reducing the differentiation of osteoclasts and by regulating the Rankl/Nlrp3/Opg pathway.
本研究评估了岩藻糖苷对骨缺损修复的有益作用及其可能的分子机制。
在本实验研究中，通过在大鼠胫骨上钻孔诱导骨缺损。然后给大鼠口服200或300mg/kg的岩藻糖苷，持续2周。根据骨形成评分以及血清中细胞因子和生化标志物的水平评估治疗效果。通过定量逆转录聚合酶链反应和蛋白质印迹分析测定Rankl/Nlrp3/Opg途径中相关蛋白在胫骨中的表达，并通过苏木精和伊红染色以及抗酒石酸酸性磷酸酶染色观察组织病理学变化。
在接受岩藻糖苷治疗的骨缺损大鼠中，骨形成评分提高，炎性细胞因子水平降低。生化标志物水平也有所改善，凋亡蛋白的表达亦是如此。岩藻糖苷还减弱了骨缺损大鼠胫骨组织中Rankl、Opg、Nlrp3、Runx2、Osterix和骨钙素（Oc）蛋白的表达，并逆转了异常的组织病理学变化。
这些结果表明，岩藻糖苷通过减少破骨细胞分化和调节Rankl/Nlrp3/Opg途径来改善骨缺损修复。
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