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依普黄酮在体外抑制小鼠破骨细胞的形成。

Ipriflavone inhibits murine osteoclast formation in vitro.

作者信息

Morita I, Sakaguchi K, Kurachi T, Murota S

机构信息

Department of Physiological Chemistry, Graduate School, Tokyo Medical and Dental University, Japan.

出版信息

Calcif Tissue Int. 1992;51 Suppl 1:S7-10. doi: 10.1007/BF02180242.

Abstract

Ipriflavone, one of the isoflavone derivatives, is a therapeutic drug for osteoporosis. The mechanism is thought to be the inhibition of bone resorption. In the present paper, we report that ipriflavone inhibited formation of osteoclasts from murine spleen cells co-cultured with stromal cells cloned from murine bone marrow. In this system, ipriflavone inhibited osteoclast generation in a dose-dependent manner (10(-7)-10(-5) M). Ipriflavone also inhibited prostaglandin E2 production in MC3T3-E1 cells, which are widely employed as osteoblasts. Moreover, ipriflavone inhibited the proliferation of stromal cells (10(-6)-10(-5) M), but not osteoblastic cells. These results suggest that one mechanism for the inhibitory effects of ipriflavone on bone resorption is the inhibition of osteoclast formation through inhibiting prostaglandin E2 production in osteoblasts and thereby suppressing proliferation of stromal cells.

摘要

依普黄酮是异黄酮衍生物之一,是一种治疗骨质疏松症的药物。其作用机制被认为是抑制骨吸收。在本论文中,我们报道依普黄酮抑制了与从小鼠骨髓克隆的基质细胞共培养的小鼠脾细胞中破骨细胞的形成。在这个体系中,依普黄酮以剂量依赖方式(10⁻⁷ - 10⁻⁵ M)抑制破骨细胞生成。依普黄酮还抑制了广泛用作成骨细胞的MC3T3-E1细胞中前列腺素E2的产生。此外,依普黄酮抑制基质细胞的增殖(10⁻⁶ - 10⁻⁵ M),但不抑制成骨细胞。这些结果表明,依普黄酮对骨吸收的抑制作用的一种机制是通过抑制成骨细胞中前列腺素E2的产生,从而抑制基质细胞的增殖来抑制破骨细胞的形成。

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