中文摘要：

目的研究唑来磷酸（ZOL）对破骨细胞分化中瞬时性受体电位通道（TRPV）5和活化T细胞核因子c1（NFATc1）基因表达的影响。方法小鼠单核巨噬细胞株RAW264.7细胞分为A、B两组：两组均用核因子-κB受体激活因子配体（RANKL）诱导5 d,B组在最后2 d应用10-6mol/L ZOL处理。检测破骨细胞生成及TRPV5、NFATc1基因表达情况。结果 B组新生多核破骨细胞数、吸收陷窝数目及面积分别为29.0±2.4、24.8±1.1、2 030.0±165.7μm2,均显著低于A组的56.5±4.5、49.3±0.9、3 946.7±367.5μm2（P〈0.01）。B组TRPV5、NFATc1的荧光强度也显著低于A组（P〈0.01）。B组TRPV5 mRNA及蛋白水平较A组分别降低了50.4%和37.8%（P〈0.01）;而NFATc1则分别下降了68.0%和48.4%（P〈0.01）。结论 ZOL可显著抑制破骨细胞生成和骨吸收,并下调TRPV5、NFATc1基因表达;ZOL对破骨细胞的抑制可能与其诱发的TRPV5、NFATc1表达抑制有关。

英文摘要：

Objective To explore the effect of zoledronate （ZOL） on osteoclast differentiation and expressions of transient receptor potential vaniUoid 5 channel （TRPV5） and nuclear factor of activated T-cells cytoplasmic 1 （NFATcl）. Methods RAW264.7 cells were divided into two groups for treatment with RANKL for 5 days （group A） or with additional ZOL treatment in the last 2 days of RANKL treatment （group B）. Osteoclastogenesis of the cells and the mRNA and protein expressions of TRPV5 and NFATcl after the treatments were examined. Results In group B, the number of newly generated osteoclasts （~〉3 nuclei）, number and size of dentin resorption lacunaes were 29.0 ＋ 2.4, 24.8 _＋ 1.1, and 2 030.0 -＋ 165.7 btm2, respectively, which were significantly lower than those in group A （56.5＋4.5, 49.3_＋0.9, and 3 946.7_＋367.5 ~m2, respectively, P〈 0.01）. Fluorescent intensity of TRPV5 and NFATcl were also significantly decreased in group B （P〈0.01）. Compared with those in group A, TRPV5 mRNA and protein expressions in group B were down-regulated by 50.4% and 37.8%, and those of NFATcl by 68.0% and 48.4%, respectively （P〈0.01）. Conclusion ZOL can significantly inhibit osteoclastogenesis and bone resorption, which may be attributed, at least partly, to ZOL-induced inhibition of TRPV5 and NFATcl expressions.