目的  探讨破骨细胞凋亡释放凋亡小体介导成骨活性的作用。   方法 通过小鼠（n=10）骨髓单核细胞体外诱导破骨细胞，用抗酒石酸酸性磷酸酶(TRAP)染色和细胞骨架F-actin与DAPI双标免疫荧光鉴定破骨细胞，破骨细胞与小鼠成骨细胞MC-3T3E1共培养体系，DNA片段化ELISA分析破骨细胞凋亡，凋亡小体标志物检测，骨形成标志物Real-time PCR分析，凋亡小体微小RNA (miRNA)表达谱芯片筛查。   结果  100 μmol/L 阿伦膦酸钠(ALN) 诱导成熟破骨细胞凋亡，并释放凋亡小体；Western blotting检测表明，ALN诱导凋亡小体特异性表面标志物蛋白表达增强；破骨细胞凋亡小体蛋白C3b表达增高与成骨细胞活性负相关；凋亡小体表达谱芯片筛查提示，miR-30a与骨形成标志物血清碱性磷酸酶(ALP)相关。   结论  破骨细胞凋亡释放的凋亡小体携带miR-30a抑制成骨细胞活性，凋亡小体可能参与破骨细胞与成骨细胞的对话。

Objective  To explore that whether apoptotic bodies released by osteoclasts mediate osteogenic activity.    Methods  The osteoclasts were induced from mouse（n=10）bone marrow monocytes in vitro, and were identified by tartrate resistant acid phosphatase (TRAP) staining, F-actin, and DAPI double labeling immunofluorescence. The Co-culture system of osteoclasts and mouse osteoblasts MC-3T3E1 was established. The apoptosis of osteoclasts was analyzed by DNA fragment ELISA. Immunoblotting of apoptotic body markers was investigated. Real-time PCR analysis of bone formation markers was tested. MiRNA expression profiling of apoptotic body was identisfied.    Results  Alendronate (ALN) 100 μmol/L induced osteoclast apoptosis and caused apoptotic body release from osteoclasts. The expression of C3b and annexin Ⅴ protein was enhanced by ALN; the expression of C3b in osteoclasts was negatively correlated with the activity of osteoblasts; the microarray screening of apoptotic body showed that miR-30a was correlated with bone formation markers and serum alkaline phosphatase (ALP).    Conclusion  Osteoclast-derived apoptotic body miR-30a can inhibit the activity of osteoblasts. Apoptotic body may participate in the dialogue between osteoclasts and osteoblasts.