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首页> 外文期刊>Journal of Cellular Physiology >Azithromycin suppresses human osteoclast formation and activity in vitro
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Azithromycin suppresses human osteoclast formation and activity in vitro

机译：阿奇霉素抑制人类破骨细胞的形成在体外和活动

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Azithromycin is an antibiotic with anti-inflammatory properties used as an adjunct to treat periodontitis, a common inflammatory mediated condition featuring pathologic alveolar bone resorption. This study aimed to determine the effect of azithromycin on human osteoclast formation and resorptive activity in vitro. Osteoclasts were generated from peripheral blood mononuclear cells stimulated with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B (RANK) ligand. The effects of azithromycin at concentrations ranging from 0.5 to 40??g/ml were tested. Osteoclast formation and activity, acidification, actin ring formation and expression of mRNA, and protein encoding for key osteoclast genes were assessed. The results demonstrated that azithromycin reduced osteoclast resorptive activity at all concentrations tested with osteoclast formation being significantly reduced at the higher concentrations (20 and 40??g/ml). mRNA and protein expression of key osteoclast transcription factor Nuclear Factor of Activated T cells (NFATc1) was significantly reduced by azithromycin at later stages of osteoclast development (day 17). Azithromycin also reduced tumor necrosis factor receptor associated factor-6 (TRAF6) mRNA expression at day 14, and cathepsin K mRNA expression at days 14 and 17. Integrin ??3 and MMP-9 mRNA expression was reduced by azithromycin at day 17 in osteoclasts cultured on dentine. The osteoclast proton pump did not appear to be affected by azithromycin, however formation of the actin ring cytoskeleton was inhibited. This study demonstrates that azithromycin inhibits human osteoclast function in vitro, which may account for at least some of the beneficial clinical effects observed with azithromycin treatment in periodontitis. J. Cell. Physiol. ? 2012 Wiley Periodicals, Inc.
机译：阿奇霉素是抗生素抗炎作用作为兼职治疗牙周炎,一种常见的炎症以病理肺泡介导的条件骨吸收。阿奇霉素对人类破骨细胞的影响在体外形成和再吸收的活动。从外周血破骨细胞生成单核细胞和巨噬细胞刺激集落刺激因子(csf)和受体核转录因子的激活卡巴B(排名)配体。浓度从0.5到40 ? ?测试。酸化,肌动蛋白形成和打电话的mRNA的表达,和蛋白质编码的关键破骨细胞基因进行评估。证明了阿奇霉素减少破骨细胞再吸收的浓度测试活动破骨细胞的形成是显著的浓度越高(20和减少40 ? ? g / ml)。破骨细胞转录因子核因子显著激活T细胞(NFATc1)减少后期的阿奇霉素破骨细胞发展(17天)。也减少了肿瘤坏死因子受体相关factor-6 (TRAF6) mRNA的表达第14天,组织蛋白酶K mRNA表达在天14和17。降低了阿奇霉素在天17吗破骨细胞培养在牙本质。质子泵似乎并未受到影响阿奇霉素,然而形成肌动蛋白的戒指细胞骨架是抑制。表明阿奇霉素抑制人类体外破骨细胞功能,这两个因素可以解释至少一些有益的临床用阿奇霉素治疗效果观察牙周炎。期刊、公司。

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