中文摘要：

目的观察成骨细胞在压应力下关键基因表达的变化及对前体破骨细胞的诱导作用,揭示压应力对骨吸收的调节机制。方法将小鼠成骨细胞系MC3T3-E1加入Ⅰ型胶原凝胶三维培养系统,给予2g/cm2压应力加载,以荧光共聚焦显微镜观察细胞形态,qPCR及ELISA分析压应力加载后核因子κB受体活化因子配体（receptor activator for nuclear factor-κB ligand,RANKL）及骨保护素（osteoprotegerin,OPG）表达的变化,并以压应力下MC3T3-E1培养上清液诱导培养小鼠单核巨噬细胞RAW264.7,检测诱导培养后其抗酒石酸酸性磷酸酶（tartrateresistant acid phosphatase,TRAP）活性的变化。结果 MC3T3-E1在压应力加载条件下依然保持了明显的三维生长形态,RANKL mRNA的表达显著上调（P〈0.05）,OPG mRNA的表达受到抑制（P〈0.05）;MC3T3-E1培养上清液中RANKL的浓度上升（P〈0.05）,OPG浓度无明显变化（P〉0.05）;受压应力加载的MC3T3-E1培养上清液可促进RAW264.7 TRAP酶活性的提高（P〈0.05）。结论压应力可能通过诱导成骨细胞上调RANKL表达并抑制OPG表达,以促进破骨细胞的分化。

英文摘要：

Objective To investigate the expression change of key genes in osteoblasts under stress and induction of it on the osteoclast precursors in order to reveal the adjustment mechanism of the compressive stress on the bone resorption.Methods The mouse osteoblastic cell line MC3T3-E1 was put into type Ⅰ collagen gel three-dimensional culture system and given 2 g / cm2 compressive stress load. Cell morphology was observed by fluorescence confocal microscopy. The expression changes of receptor activator for nuclear factor-κ B ligand（RANKL） and osteoprotegerin（OPG） after stress load was analyzed by quantitative real-time PCR and ELISA. The mouse monocyte-macrophage cells RAW264. 7 was induced cultured by MC3T3-E1 culture supernatants under stress, whose tartrate-resistant acid phosphatase, TRAP activity change was detected after the induced culture. Results Under compressive stress load, MC3T3-E1 kept an obvious three-dimensional growth morphology, RANKL mRNA expression was significantly up-regulated（P〈0. 05）, whereas OPG mRNA expression was inhibited（P〈0. 05）; MC3T3-E1 RANKL concentration in the culture supernatant increased（P〈0. 05）, there was no significant change on the OPG concentration（P〈0. 05）; MC3T3-E1 culture supernatants under compressive stress load could promote the improvement of RAW264. 7 TRAP activity（P〈0. 05）. Conclusion Stress can promote osteoclasts differentiation by inducing osteoblasts up-regulating RANKL expression and inhibiting OPG expression.