脱氢表雄酮抑制骨吸收的作用机制

 目的　研究脱氢表雄酮 (DHEA)治疗绝经后骨质疏松的作用机制。方法　体外分离和培养成骨细胞和破骨细胞 ,在有或无成骨细胞存在的条件下,观察10^-7mol·L^-1 的DHEA对破骨细胞骨吸收作用的影响;经DHEA作用1,2,3d后 ,半定量RT-PCR测定护骨素/核因子κB受体活化因子配基(OPG/RANKL)的mRNA水平。结果　 10^-7mol·L^-1 的DHEA能明显增加成骨细胞OPG/RANKL的mRNA比值(P<0.01) ;当成骨细胞存在时,DHEA可以减少骨吸收陷窝的数目(P<0.05)和面积 (P<0.01)。结论　DHEA只有在成骨细胞存在时可以抑制破骨细胞的骨吸收作用,该作用可能通过间接调节成骨细胞OPG/RANKL的转录而介导。

Inhibition mechanism of bone resorption by dehydroepiandrosterone

OBJECTIVE To investigate the action mechanism of dehydroepiandrosterone in postmenopausal osteoporosis therapy. METHODS Osteoblast (OB) and osteoclast (OC) were isolated and cultured, then the action of dehydroepiandrosterone (10^-7mol·L^-1) on bone resorption of OC in the presence or absence of OB was observed. The number and area of absorption lacuna of cattle slice were measured. The level of OPG/RANKL mRNA of OB cultured with DHEA was determined semiquantitatively. RESULTS DHEA apparently increased the ratio of OPG/RANKL mRNA (P<0.01) in OBs in the presence of OBs, and decreased the number (P<0.05) and area (P<0.01) of the absorption lacuna of specula. CONCLUSION Only in the presence of OB, can DHEA inhibit the bone resorption of OC, which may be mediated by OPG/RANKL of OB.