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青蒿琥酯在体外抑制核因子κB受体活化因子配体(RANKL)诱导的破骨细胞生成和骨吸收,并在体内预防脂多糖(LPS)诱导的骨质流失。

Artesunate inhibits RANKL-induced osteoclastogenesis and bone resorption in vitro and prevents LPS-induced bone loss in vivo.

作者信息

Wei Cheng-Ming, Liu Qian, Song Fang-Ming, Lin Xi-Xi, Su Yi-Ji, Xu Jiake, Huang Lin, Zong Shao-Hui, Zhao Jin-Min

机构信息

Research Centre for Regenerative Medicine and Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi, China.

Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, Guangxi, China.

出版信息

J Cell Physiol. 2018 Jan;233(1):476-485. doi: 10.1002/jcp.25907. Epub 2017 Aug 17.

Abstract

Osteoclasts are multinuclear giant cells responsible for bone resorption in lytic bone diseases such as osteoporosis, arthritis, periodontitis, and bone tumors. Due to the severe side-effects caused by the currently available drugs, a continuous search for novel bone-protective therapies is essential. Artesunate (Art), the water-soluble derivative of artemisinin has been investigated owing to its anti-malarial properties. However, its effects in osteoclastogenesis have not yet been reported. In this study, Art was shown to inhibit the nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis, the mRNA expression of osteoclastic-specific genes, and resorption pit formation in a dose-dependent manner in primary bone marrow-derived macrophages cells (BMMs). Furthermore, Art markedly blocked the RANKL-induced osteoclastogenesis by attenuating the degradation of IκB and phosphorylation of NF-κB p65. Consistent with the in vitro results, Art inhibited lipopolysaccharide (LPS)-induced bone resorption by suppressing the osteoclastogenesis. Together our data demonstrated that Art inhibits RANKL-induced osteoclastogenesis by suppressing the NF-κB signaling pathway and that it is a promising agent for the treatment of osteolytic diseases.

摘要

破骨细胞是多核巨细胞,在骨质疏松症、关节炎、牙周炎和骨肿瘤等溶骨性骨疾病中负责骨吸收。由于现有药物会引起严重的副作用,持续寻找新型骨保护疗法至关重要。青蒿琥酯(Art)是青蒿素的水溶性衍生物,因其抗疟疾特性而受到研究。然而,其在破骨细胞生成中的作用尚未见报道。在本研究中,Art在原代骨髓来源的巨噬细胞(BMMs)中呈剂量依赖性地抑制核因子κB配体(RANKL)诱导的破骨细胞生成、破骨细胞特异性基因的mRNA表达以及吸收陷窝的形成。此外,Art通过减弱IκB的降解和NF-κB p65的磷酸化,显著阻断RANKL诱导的破骨细胞生成。与体外结果一致,Art通过抑制破骨细胞生成来抑制脂多糖(LPS)诱导的骨吸收。我们的数据共同表明,Art通过抑制NF-κB信号通路来抑制RANKL诱导的破骨细胞生成,并且它是一种治疗溶骨性疾病的有前景的药物。

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