细菌脂多糖对破骨细胞发育的抑制作用研究  

Inhibition of osteoclast differentiation by lipopolysaccharide

作　　者：赵为公[1] 王莹[1] 邱希江[1] 白斌[1] 邱裕生[1] 

机构地区：[1]西安交通大学第一附属医院骨科,陕西西安710061

出　　处：《中日友好医院学报》2013年第1期30-33,F0002,共5页Journal of China-Japan Friendship Hospital

摘　　要：目的:寻找调节破骨细胞分化成熟的途径。方法:采用细胞核因子-κB受体活化因子配体(RANKL)和巨噬细胞集落刺激因子(M-CSF)体外诱导骨髓单核细胞分化为成熟破骨细胞的培养方法,在培养体系中加入不同浓度细菌脂多糖(LPS),用抗酒石酸酸性磷酸酶(TRAP)染色观察成熟破骨细胞形成情况;实时定量RT-PCR检测LPS处理后破骨细胞前体表达核因子-κB受体活化因子(RANK)和M-CSF受体mRNA。结果:LPS不能刺激骨髓单核细胞形成TRAP阳性的破骨细胞;减少了RANKL诱导的TRAP阳性破骨细胞形成数量;0.2ng/ml和20ng/ml LPS降低了30%和90%RANKL诱导TRAP阳性细胞形成数量(与未加LPS组比较,均P<0.01);降低破骨细胞前体表达RANK和M-CSFR mRNA。结论:LPS能够抑制RANKL诱导的破骨细胞分化成熟,抑制破骨细胞前体表达RANK和M-CSFR,能够阻断其向成熟分化。Objective：To study inhibition of osteoclast differentiation by lipopolysaccharide（LPS）.Methods：Osteoclast cells were prepared in the present of receptor activator of nuclear factor-κB ligand（RANKL）and macrophage colony-stimulating factor（M-CSF）from bone marrow mononuclear cells.Tartrate-resistant acid phosphatase（TRAP）staining observed osteoclastogenic activity induced by different concentration of LPS.RT-PCR was used to detect RANK and macrophage colony-stimulating factor,M-CSF receptor expression in precursor osteoclast cells.Results：LPS could reduce osteoclast differentiation in precursor osteoclast cells,inhibition of 30% TRAP（＋） osteoclasts（P0.01）was observed at 0.2ng/ml and 90% inhibition（P0.01）was observed at 20ng/ml.LPS decreased the expression of receptor activator of nuclear factor-κB（RANK）and M-CSF receptor in osteoclast precursors.Conclusion：LPS inhibited RANKL-induced osteoclastogenesis activity by reducing the expression of RANK and M-CSF receptor.

关 键 词：破骨细胞 细菌脂多糖 核因子-κB受体活化因子 巨噬细胞集落刺激因子受体 

分 类 号：R329[医药卫生—人体解剖和组织胚胎学]