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.

中文翻译：

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Corilagin通过NF-κB和PI3K / AKT信号通路抑制RANKL诱导的破骨细胞生成并抑制雌激素缺乏引起的骨丢失。

由炎症引起的过度活化的破骨细胞形成与骨质疏松症有关。Corilagin，一种从多种药用草本植物（如肉桂）中提取的天然化合物，具有抗氧化和抗炎活性。我们发现Corilagin以剂量依赖性方式抑制破骨细胞分化，显着降低了破骨细胞相关基因的表达，并破坏了破骨细胞对骨的吸收。此外，Corilagin可减少核因子-κB（NF-κB）和PI3K / AKT信号通路成员的磷酸化。在骨质疏松症的小鼠模型中，Corilagin可抑制体内的破骨细胞功能并恢复雌激素缺乏症引起的骨质流失。总之，我们的发现表明，Corilagin通过下调NF-κB和PI3K / AKT信号传导通路抑制破骨细胞生成，从而显示出其治疗骨质疏松症的潜在可能性。