摘要
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 0 1) ;当成骨细胞存在时 ,DHEA可以减少骨吸收陷窝的数目 (P <0 0 5 )和面积 (P <0 0 1)。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。
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 (10-7 mol·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.
出处
《中国药学杂志》
EI
CAS
CSCD
北大核心
2004年第6期429-431,共3页
Chinese Pharmaceutical Journal
基金
上海市科技发展基金 (0 0 40 190 61)
