Bu-Shen-Ning-Xin decoction suppresses osteoclastogenesis via increasing dehydroepiandrosterone to prevent postmenopausal osteoporosis
Bu-Shen-Ning-Xin decoction suppresses osteoclastogenesis via increasing dehydroepiandrosterone to prevent postmenopausal osteoporosis
复制标题
补肾宁心汤通过增加脱氢表雄酮抑制破骨细胞生成预防绝经后骨质疏松
DOI：
10.5582/bst.2015.01011
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发表时间：
2015-06-01
影响因子：
5.5
通讯作者：
Wang, Ling
中科院分区：
文献类型：
--
作者：
Gui, Yuyan;Qiu, Xuemin;Wang, Ling
补肾宁心汤是一种传统中药，用于预防和治疗绝经后骨质疏松症等与年龄相关的疾病已有几十年的历史。由于骨吸收在骨质疏松症的发生和进展中起关键作用，本研究旨在研究BSNXD在体外核因子κ B配体（RANKL）诱导破骨细胞生成的受体活化方面的潜在机制。在小鼠中，血清脱氢表雄酮（DHEA），硫酸脱氢表雄酮（DHEAS），和17-β-雌二醇（E2）的水平进行了评价与酶免疫试剂盒卵巢切除术后。BSNXD给药后，DHEA和DHEAS水平显著升高，而E2水平则无明显变化。此外，抗酒石酸酸性磷酸酶染色显示，DHEA通过雌激素受体α（ER α）而非雌激素受体β或雄激素受体以剂量依赖性方式在体外显著抑制RANKL诱导的破骨细胞生成。在3-（4，5-二甲基噻唑-2-基）-2，5-二苯基溴化四唑（MTT）试验中未检测到细胞毒性。这些数据表明，BSNXD预防PMO通过增加DHEA通过ER α途径抑制破骨细胞生成。
Bu-Shen-Ning-Xin decoction (BSNXD), a traditional Chinese medicine, has been used to prevent and treat age-related diseases such as postmenopausal osteoporosis (PMO) for decades. This study sought to investigate the underlying mechanisms of BSNXD in terms of receptor activation of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis in vitro because of the critical roles of bone resorption in the development and progression of osteoporosis. In mice, serum levels of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), and 17-beta-estradiol (E2) were evaluated with an enzyme immunoassay kit after ovariectomy. Levels of DHEA and DHEAS increased significantly following administration of BSNXD while the level of E2 did not. In addition, tartrate-resistance acid phosphatase staining showed that DHEA profoundly inhibited RANKL-induced osteoclastogenesis in vitro in a dose-dependent manner via estrogen receptor alpha (ER alpha) but not via estrogen receptor beta or androgen receptors. Cytotoxicity was not detected in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. These data suggest that BSNXD prevents PMO by increasing DHEA via the ERa pathway to suppress osteoclastogenesis.