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卡诺醇可减轻体外 RANKL 诱导的破骨细胞生成和 LPS 诱导的骨丢失。

Carnosol attenuates RANKL-induced osteoclastogenesis in vitro and LPS-induced bone loss.

机构信息

Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, No. 88, Jiefang Road, Hangzhou 310009, China; Orthopedics Research Institute of Zhejiang University, No. 88, Jiefang Road, Hangzhou 310009, China.

Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, No. 88, Jiefang Road, Hangzhou 310009, China; Orthopedics Research Institute of Zhejiang University, No. 88, Jiefang Road, Hangzhou 310009, China.

出版信息

Int Immunopharmacol. 2020 Dec;89(Pt A):106978. doi: 10.1016/j.intimp.2020.106978. Epub 2020 Oct 8.

DOI:10.1016/j.intimp.2020.106978
PMID:33039968
Abstract

Osteolysis is characterized by the imbalance of bone remodeling triggered by excessive activation of osteoclasts, which ultimately leads to pathological bone destruction. Diseases caused by overactive osteoclasts, such as osteolysis around the prosthesis, periodontitis and osteoporosis, are clinically common but lack effective treatment. Therefore, exploring regimens that could specifically impair the formation and function of osteoclasts has become a breakthrough in the treatment of these diseases. Carnosol is a natural phenolic diterpene with anti-inflammatory, antibacterial, anti-tumor and antioxidant properties. In this study, we found that carnosol can impede RANKL-induced osteoclastogenesis via modulating the activation of NF-κb and JNK signaling pathways in vitro. Additionally, we confirmed that carnosol could alleviate bone loss in amurine model of LPS-induced inflammatory bone erosion in vivo. Thence, these findings demonstrate that carnosol may be a potentially effective regent for the treatment of osteoclast-related disorders.

摘要

骨溶解的特征在于破骨细胞过度激活引发的骨重建失衡,最终导致病理性骨破坏。由破骨细胞过度活跃引起的疾病,如假体周围骨溶解、牙周炎和骨质疏松症,在临床上很常见,但缺乏有效的治疗方法。因此,探索专门损害破骨细胞形成和功能的方案已成为治疗这些疾病的突破点。龙舌兰醇是一种具有抗炎、抗菌、抗肿瘤和抗氧化特性的天然酚类二萜。在这项研究中,我们发现龙舌兰醇可以通过调节 NF-κb 和 JNK 信号通路的激活来抑制 RANKL 诱导的破骨细胞发生。此外,我们还证实龙舌兰醇可以减轻体内 LPS 诱导的炎症性骨侵蚀小鼠模型中的骨丢失。因此,这些发现表明龙舌兰醇可能是一种治疗破骨细胞相关疾病的潜在有效药物。

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