CAJ | 학술논문

目的研究唑来膦酸对破骨细胞分化及信号分子钙调蛋白、钙调蛋白依赖性激酶(calmodulin-dependent protein kinase,CAMK)Ⅱ基因表达的影响.方法应用核因子κB受体激活蛋白配体(receptor activatior of nuclear factor κB ligand,RANKL)诱导小鼠单核巨噬细胞株RAW264.7向破骨细胞分化.细胞分为两组:A组用RANKL诱导5 d;B组在RANKL诱导3d后加用唑来膦酸处理2d.检测破骨细胞生成及钙调蛋白、CAMKⅡ基因表达情况.结果 B组新生多核破骨细胞、吸收陷窝数目及面积分别为(23±3)、(19±2)和(4951±223) μm2,均显著低于A组的(44±3)、(46±1)和(13 331±248) μm2 (P ＜0.01).与A组比较,B组钙调蛋白、CAMKⅡ基因表达也显著下降(P＜0.01),mRNA及蛋白水平钙调蛋白分别下降了26.7％和37.2％；CAMKⅡ分别下降了57.0％和76.1％.结论唑来膦酸可显著抑制破骨细胞生成和骨吸收功能,并下调钙调蛋白、CAMKⅡ基因表达；信号分子钙调蛋白、CAMKⅡ可能参与了唑来膦酸对破骨细胞的抑制作用.
목적 연구서래련산대파골세포분화급신호분자개조단백、개조단백의뢰성격매(calmodulin-dependent protein kinase,CAMK)Ⅱ기인표체적영향.방법 응용핵인자κB수체격활단백배체(receptor activatior of nuclear factor κB ligand,RANKL)유도소서단핵거서세포주RAW264.7향파골세포분화.세포분위량조:A조용RANKL유도5 d;B조재RANKL유도3d후가용서래련산처리2d.검측파골세포생성급개조단백、CAMKⅡ기인표체정황.결과 B조신생다핵파골세포、흡수함와수목급면적분별위(23±3)、(19±2)화(4951±223) μm2,균현저저우A조적(44±3)、(46±1)화(13 331±248) μm2 (P ＜0.01).여A조비교,B조개조단백、CAMKⅡ기인표체야현저하강(P＜0.01),mRNA급단백수평개조단백분별하강료26.7％화37.2％；CAMKⅡ분별하강료57.0％화76.1％.결론 서래련산가현저억제파골세포생성화골흡수공능,병하조개조단백、CAMKⅡ기인표체；신호분자개조단백、CAMKⅡ가능삼여료서래련산대파골세포적억제작용.
Objective To investigate the effect of zoledronate acid on osteoclast differentiation and gene expression of calmodulin (CAM) and calmodulin-dependent protein kinase (CAMK) Ⅱ.Methods Receptor activatior of nuclear factor κB ligand (RANKL) was used to induce differentiation of RAW264.7cells into osteoclasts in vitro.The cells were divided into two groups,group A and group B.Both groups were treated with RANKL for 5 days,whereas group B was also treated with zoledronate for the last 2 days.Osteoclastogenesis and gene expression of CAM and CAMK Ⅱ were examined.Results In group B,the number of new-generated osteoclasts (≥ 3 nuclei),number and size of dentin resorption lacunaes were (23 ±3),(19 ±2) and (4951 ±223) μm2 respevtively,which were significantly lower than those [(44 ±3),(46±1) and (13 331 ±248) μ m2]in group A (P＜0.01).mRNA and protein level of CAM and CAMK Ⅱ were also significantly down-regulated in group B when compared with group A (P ＜ 0.01) and the decrease was 26.7％ and 37.2％ respectively for CAM,57.0％ and 76.1％ respectively for CAMK Ⅱ.Conclusions Zoledronate acid could significantly inhibit formation and resorption function of osteoclasts.CAM and CAMK Ⅱ may be involved in the inhibition process.