Kim Kwang-Jin, Lee Yong-Jin, Hwang Yun-Ho, Kang Kyung-Yun, Yee Sung-Tae, Son Young-Jin
Department of Pharmacy, Sunchon National University, Jeonnam, Suncheon 57922, Korea.
J Clin Med. 2017 Mar 14;6(3):32. doi: 10.3390/jcm6030032.
Bone remodeling, a physiological process characterized by bone formation by osteoblasts and bone resorption by osteoclasts, is important for the maintenance of healthy bone in adult humans. Osteoclasts play a critical role in bone erosion and osteoporosis and are bone-specific multinucleated cells generated through differentiation of monocyte/macrophage lineage precursors. Receptor activator of NF-κB ligand (RANKL) has been reported to induce osteoclast differentiation. In this study, we explored whether Gracilaria verrucosa extracts (GE) could affect RANKL-mediated osteoclast differentiation. GE significantly inhibited RANKL-activated osteoclast differentiation by inhibiting protein expression of c-fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), vital factors in RANKL-mediated osteoclastogenesis. In addition, GE attenuated ovariectomy-induced bone loss in mice. In summary, GE can prevent osteoclastogenesis and hormone-related bone loss via blockage of c-fos-NFATc1 signaling. Our results suggest that GE may have therapeutic potential in the treatment of postmenopausal osteoporosis.
骨重塑是一个以成骨细胞形成骨和破骨细胞吸收骨为特征的生理过程,对维持成年人体内健康骨骼很重要。破骨细胞在骨侵蚀和骨质疏松中起关键作用,是通过单核细胞/巨噬细胞谱系前体分化产生的骨特异性多核细胞。据报道,核因子κB受体活化因子配体(RANKL)可诱导破骨细胞分化。在本研究中,我们探讨了江蓠提取物(GE)是否会影响RANKL介导的破骨细胞分化。GE通过抑制RANKL介导的破骨细胞生成中的关键因子c-fos和活化T细胞核因子细胞质1(NFATc1)的蛋白表达,显著抑制RANKL激活的破骨细胞分化。此外,GE减轻了去卵巢诱导的小鼠骨质流失。总之,GE可通过阻断c-fos-NFATc1信号通路预防破骨细胞生成和激素相关的骨质流失。我们的结果表明,GE在治疗绝经后骨质疏松症方面可能具有治疗潜力。