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脱氢表雄酮通过上调骨保护素/核因子κB受体活化因子配体抑制骨吸收。

Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL.

作者信息

Wang Yu Dong, Wang Ling, Li Da Jin, Wang Wen Jun

机构信息

Department of Obstetrics and Gynecology, the Sixth People's Hospital, Jiaotong University, Shanghai, China.

出版信息

Cell Mol Immunol. 2006 Feb;3(1):41-5.

PMID:16549048
Abstract

The plasma level of dehydroepiandrosterone (DHEA) decreases gradually along with aging. The beneficial effects of DHEA as an anti-aging steroid, such as the stimulatory effect on immune system, anti-diabetes mellitus, anti-atherosclerosis, anti-dementia, anti-obesity and anti-osteoporosis have been demonstrated in experiment both in vitro and in vivo. It is important to investigate the effective mechanism of DHEA in therapeutics for postmenopausal osteoporosis. Having isolated and cultured osteoblasts (OBs) and osteoclasts (OCs), we analysed the effect of DHEA on osteoblastic viability, regulation of DHEA on the expression of osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) mRNA in OBs, and then observed the action of DHEA on bone resorption of OCs in the presence or absence of OBs. The results showed that DHEA improved viability of OBs within the concentration range of 0.01-1 microM, especially at the concentration of 0.1 microM. DHEA could apparently increase the ratio of OPG/RANKL mRNA in OBs. In the presence of OBs, DHEA could decrease the number and area of absorption lacuna of specula. We concluded, therefore, only in the presence of OBs, DHEA could inhibit the bone resorption of OCs, which may be mediated by OPG/RANKL of OBs.

摘要

脱氢表雄酮(DHEA)的血浆水平会随着衰老而逐渐降低。DHEA作为一种抗衰老类固醇的有益作用,如对免疫系统的刺激作用、抗糖尿病、抗动脉粥样硬化、抗痴呆、抗肥胖和抗骨质疏松等,已在体外和体内实验中得到证实。研究DHEA治疗绝经后骨质疏松症的有效机制具有重要意义。我们分离培养了成骨细胞(OBs)和破骨细胞(OCs),分析了DHEA对成骨细胞活力的影响、DHEA对成骨细胞中骨保护素(OPG)/核因子κB受体活化因子配体(RANKL)mRNA表达的调控,然后观察了在有无成骨细胞存在的情况下DHEA对破骨细胞骨吸收的作用。结果表明,在0.01 - 1微摩尔浓度范围内,尤其是在0.1微摩尔浓度时,DHEA提高了成骨细胞的活力。DHEA能明显增加成骨细胞中OPG/RANKL mRNA的比例。在有成骨细胞存在的情况下,DHEA能减少骨片吸收陷窝的数量和面积。因此,我们得出结论,只有在有成骨细胞存在时,DHEA才能抑制破骨细胞的骨吸收,这可能是由成骨细胞的OPG/RANKL介导的。

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