<br>C-藻蓝蛋白通过抑制 ROS 水平、NFATc1 和 NF-κB 激活，在体外减弱 RANKL 诱导的破骨细胞生成和骨吸收。,Scientific Reports

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C-藻蓝蛋白通过抑制 ROS 水平、NFATc1 和 NF-κB 激活，在体外减弱 RANKL 诱导的破骨细胞生成和骨吸收。
Scientific Reports ( IF 3.8 ) Pub Date : 2020-02-13 , DOI: 10.1038/s41598-020-59363-y
Mohammed S AlQranei _{1,

2} , Hanan Aljohani _{1,

3} , Sunipa Majumdar ₁ , Linda T Senbanjo ₁ , Meenakshi A Chellaiah ₁

Affiliation

过度骨质流失发生在牙周炎和骨质疏松症等炎症性疾病中。其潜在机制与巨噬细胞分化为多核巨型破骨细胞及其骨吸收活性有关。 C-藻蓝蛋白（C-PC）是从蓝绿藻中提取的藻胆蛋白，已被证明具有多种药理作用。 C-PC对骨代谢的作用有待揭示。在这项研究中，我们确定了 C-PC 作为破骨细胞分化、活性和体外存活抑制剂的有效性。我们发现，C-PC 强烈抑制巨噬细胞向 TRAP 阳性破骨细胞的分化、独特的破骨细胞特异性足体组织和牙本质基质吸收，而没有任何细胞毒性。此外，它还能在 mRNA 和蛋白质水平上抑制破骨细胞特异性标记物的表达，例如组织蛋白酶 K 和整合素 β3。 RANKL 介导的信号传导利用活性氧 (ROS) 来分化破骨细胞。 C-PC 减弱 RANKL 刺激的 ROS。机制研究表明，C-PC 有可能通过阻断胞质 IκB-α 的降解来减少破骨细胞的形成，从而阻断下游标记物（如 c-Fos 和 NFATc1）的激活。然而，它对体外成骨细胞介导的骨形成没有任何影响。总的来说，我们的数据表明，C-PC 可用作一种治疗剂，可以针对破骨细胞过度骨吸收介导的骨丢失，而不影响骨中的成骨细胞活性。

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C-phycocyanin attenuates RANKL-induced osteoclastogenesis and bone resorption in vitro through inhibiting ROS levels, NFATc1 and NF-κB activation.

Excessive bone loss occurs in inflammatory disorders such as periodontitis and osteoporosis. The underlying mechanism is related to the differentiation of macrophages into multinucleated giant osteoclasts and their bone resorptive activity. C-Phycocyanin (C-PC) is a phycobiliprotein extracted from the blue-green algae, which has been shown to have various pharmacological effects. The role of C-PC on bone metabolism needs revelation. In this study, we determined the effectiveness of C-PC as an inhibitor of osteoclast differentiation, activity, and survival in vitro. We found that C-PC strongly inhibited the differentiation of macrophages to TRAP-positive osteoclasts, distinctive osteoclast specific podosomal organization, and dentine matrix resorption without any cytotoxicity. Also, it suppressed the expression of osteoclast specific markers, such as cathepsin K and integrin β3 at mRNA and protein levels. RANKL mediated signaling utilizes reactive oxygen species (ROS) for the differentiation of osteoclasts. C-PC attenuated RANKL stimulated ROS. Mechanistic studies indicate that C-PC has the potential to reduce osteoclast formation via blocking the degradation of cytosolic IκB-α and hence, the activation of downstream markers such as c-Fos and NFATc1. However, it does not have any effect on osteoblast-mediated bone formation in vitro. Collectively, our data suggest that C-PC may be utilized as a therapeutic agent that can target bone loss mediated by excessive osteoclastic bone resorption without affecting osteoblastic activity in bone.

更新日期：2020-02-13

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