核因子κB受体活化因子配体对唑来膦酸诱发的破骨细胞生成及NF-κB p50和c-Jun基因表达抑制的挽救效应

发布时间：2018-09-11 06:08

【摘要】：研究核因子κB受体活化因子配体(RANKL)对唑来膦酸(ZOL)诱发的破骨细胞生成及NF-κB p50和cJun基因表达抑制的挽救效应。体外分离小鼠颅骨成骨细胞(OB),并与RAW264.7细胞共培养。将细胞分为4组,给予ZOL和RANKL处理;于不同时间点检测破骨细胞(OC)生成及NF-κB p50和c-Jun基因表达情况。B组(ZOL组)TRAP阳性多核OC及吸收陷窝最少(P0.05或P0.01),其次为C组(ZOL+RANKL组),D组(RANKL组)OC及吸收陷窝最多,与A组(对照)相似(P0.05)。NF-κB p50和c-Jun基因表达也是B组最低(P0.05或P0.01),而C组较B组显著升高(P0.05),A组和D组基因表达最高且表达水平相近(P0.05)。实验结果表明,RANKL可以在共培养体系中部分挽救ZOL对OC生成的抑制作用;而NF-κB p50和c-Jun可能介导了RANKL和ZOL对OC的上述效应。
[Abstract]:To study the rescue effect of nuclear factor 魏 B receptor activating factor (RANKL) ligand on osteoclast formation induced by zoledronate (ZOL) and the expression of NF- 魏 B p50 and cJun genes. (OB), of mouse skull osteoblasts was isolated in vitro and co-cultured with RAW264.7 cells. The cells were divided into 4 groups and treated with ZOL and RANKL. (OC) production of osteoclasts and the expression of NF- 魏 B p50 and c-Jun genes in osteoclasts were detected at different time points. Group B (ZOL group) had the least TRAP positive polynuclear OC and resorption lacunae (P0.05 or P0.01), followed by C group (ZOL RANKL group (RANKL group) and D group (RANKL group). Similar to group A (P0.05), the expression of p50 and c-Jun of NF- 魏 B was also the lowest in group B (P0.05 or P0.01), while the expression of p50 and c-Jun in group C was significantly higher than that in group B (P0.05). The expression level of p50 and c-Jun in group A and D was the highest and similar (P0.05). The results showed that RANKL could partially save the inhibitory effect of ZOL on OC production in co-culture system, while NF- 魏 B p50 and c-Jun might mediate the above effects of RANKL and ZOL on OC.
【作者单位】：河北联合大学口腔医学院;
【基金】：国家自然科学基金资助项目(81270965) 河北省自然科学基金资助项目(C2011401044)
【分类号】：R329.2

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