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首页> 外文期刊>Experimental and therapeutic medicine >Alendronate promotes osteoblast differentiation and bone formation in ovariectomy-induced osteoporosis through interferon-beta/signal transducer and activator of transcription 1 pathway
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Alendronate promotes osteoblast differentiation and bone formation in ovariectomy-induced osteoporosis through interferon-beta/signal transducer and activator of transcription 1 pathway

机译：Alendronate通过干扰素-β/信号传感器和转录1途径激活剂促进卵巢切除术诱导的骨质疏松症的成骨细胞分化和骨形成

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摘要

Alendronate is commonly used for the treatment of postmenopausal osteoporosis; however, the underlying pathological molecular mechanisms of its action remain unclear. In the present study, the alendronate-treated signaling pathway in bone metabolism in rats with ovariectomy induced by osteoporosis was investigated. Rats with osteoporosis were orally administered alendronate or phosphate-buffered saline (control). In addition, the interferon-beta (IFN-beta)/signal transducer and activator of transcription 1 (STAT1) signaling pathway was investigated in osteoblasts following treatment with alendronate in vitro and in vivo. During the differentiation period, IFN-beta (100 ng/ml) was used to treat the osteoblast cells, and the activity, viability and bone metabolism-associated gene expression levels (STAT1, p-STAT1, Fra1, TRAF6 and SOCS1) were analyzed in osteoblast cells. Histopathological changes were used to evaluate osteoblasts, osteoclasts, inflammatory phase of bone healing and osteonecrotic areas. The results demonstrated that alendronate significantly inhibited the activity of osteoporotic osteoclasts by stimulating expression of IFN-beta, as well as markedly improved the viability and activity of osteoblasts compared with the control group. In addition, alendronate increased the expression and phosphorylation levels of STAT1 in osteoclasts, enhanced osteoblast differentiation, upregulated the expression levels of alkaline phosphatase and osteocalcin, and increased the expression of osteoblast differentiation-associated genes (osteocalcin, osterix and Runx2). Inhibition of IFN-beta expression canceled the benefits of alendronate-mediated osteoblast differentiation. Notably, alendronate enhanced bone formation in rats with osteoporosis induced by ovariectomy. In conclusion, these findings suggest that alendronate can regulate osteoblast differentiation and bone formation in rats with osteoporosis induced by ovariectomy through upregulation of IFN-beta/STAT1 signaling pathway.
机译：阿仑膦酸盐通常用于治疗绝经后骨质疏松症;然而，其行动的潜在病理分子机制仍然不清楚。在本研究中，研究了通过骨质疏松症诱导的卵巢切除术大鼠骨代谢的阿仑膦酸盐处理通路。口服骨质疏松症的大鼠口服施用的醛膦酸盐或磷酸盐缓冲盐水（对照）。此外，在体外和体内用醛酸盐处理后，研究了在成骨细胞中研究了干扰素-β（IFN-β）/信号传感器和转录1（STAT1）信号通路的活化剂。在分化期间，使用IFN-β（100ng / ml）治疗成骨细胞，分析活性，活力和骨代谢相关基因表达水平（STAT1，P-STAT1，FRA1，TRAF6和SOCS1）在成骨细胞中。组织病理学变化用于评估成骨细胞，骨细胞，骨愈合和骨折分解区域的炎症期。结果表明，通过刺激IFN-β的表达，还显着抑制了骨质疏松疏松骨髓性的活性，以及​​与对照组相比显着改善成骨细胞的活力和活性。此外，Alendronate增加了疏口细胞中Stat1的表达和磷酸化水平，增强了成骨细胞分化，上调了碱性磷酸酶和骨钙素的表达水平，并增加了成骨细胞分化相关基因的表达（骨钙素，Ostrox2）。 IFN-β表达的抑制取消了醛酸酯介导的成骨细胞分化的益处。值得注意的是，卵巢切除术造成骨质疏松症的大鼠的阿仑膦酸盐增强骨形成。总之，这些研究结果表明，通过UPN-Beta / Stat1信号传导途径的上调，AlyNate可以调节卵巢切除术诱导的骨质疏松症的大鼠骨细胞分化和骨形成。

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