首页> 美国卫生研究院文献>Journal of Cellular and Molecular Medicine >Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways
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Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways

机译:Corilagin抑制Rankl诱导的骨核细胞发生并通过NF-κB和PI3K / AKT信号通路抑制雌激素缺乏诱导的骨质损失

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摘要

Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.
机译:通过炎症引发的过活性的骨质细胞发生,这一切都与骨质疏松症有关。柯尔加蛋白是一种从各种药用草本植物中提取的天然化合物,例如Cinnamomum Cassia,具有抗氧化剂和抗炎活性。我们发现核素抑制了逐渐依赖性方式的骨胶分化,显着降低了与骨细胞的骨细胞相关基因表达和骨吸收受损。此外,核因子-κB(NF-κB)和PI3K / AKT信号传导途径的磷酸化由Corilagin降低。在骨质疏松症的小鼠模型中,核素蛋白抑制了体内骨质体功能和恢复的雌激素缺乏诱导的骨质损失。总之,我们的研究结果表明,核素通过降低NF-κB和PI3K / AKT信号传导途径来抑制骨髓细胞发生,从而呈现出骨质疏松症治疗的潜在可能性。

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