Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Int Immunopharmacol. 2012 Mar;12(3):494-500. doi: 10.1016/j.intimp.2012.01.002. Epub 2012 Jan 23.
Numerous studies have indicated that inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with osteoporosis. D-pinitol, a 3-methoxy analogue of D-chiroinositol, was identified as an active principle in soy foods and legumes. Here we found that D-pinitol markedly inhibited the receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastic differentiation from bone marrow stromal cells and RAW264.7 macrophage cells. In addition, D-pinitol also reduced RANKL-induced p38 and JNK phosphorylation. Furthermore, RANKL-mediated increase of IKK, IκBα, and p65 phosphorylation and NF-κB-luciferase activity was inhibited by D-pinitol. However, D-pinitol did not affect the proliferation and differentiation of osteoblasts. In addition, D-pinitol also prevented the bone loss induced by ovariectomy in vivo. Our data suggest that D-pinitol inhibits osteoclastogenesis from bone marrow stromal cells and macrophage cells via attenuated RANKL-induced p38, JNK, and NF-κB activation, which in turn protect bone loss from ovariectomy.
大量研究表明，炎症细胞因子在破骨细胞生成中起主要作用，导致与骨质疏松症频繁相关的骨质吸收。D-松醇，D-手性肌醇的 3-甲氧基类似物，被确定为大豆食品和豆类中的一种有效成分。在这里，我们发现 D-松醇显著抑制了核因子 kappa B 配体（RANKL）诱导的骨髓基质细胞和 RAW264.7 巨噬细胞的破骨细胞分化。此外，D-松醇还降低了 RANKL 诱导的 p38 和 JNK 磷酸化。此外，RANKL 介导的 IKK、IκBα 和 p65 磷酸化和 NF-κB-荧光素酶活性也被 D-松醇抑制。然而，D-松醇并不影响成骨细胞的增殖和分化。此外，D-松醇还可预防体内去卵巢引起的骨丢失。我们的数据表明，D-松醇通过减弱 RANKL 诱导的 p38、JNK 和 NF-κB 激活来抑制破骨细胞生成，从而防止去卵巢引起的骨丢失。
