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目的研究淫羊藿苷(icariin,ICR)对雌性激素受体(estrogen receptor,ER)与地塞米松(dexamethasone,DEX)诱导的MC3T3-E1成骨抑制效应的影响。方法分别以DEX 10?5 mol·L?1、ICR 10?6 mol·L?1、雌激素(E2)10?8 mol·L?1及ICI182780(IN)10?5 mol·L?1干预MC3T3-E1成熟分化过程,并通过real-time RT-PCR、Westen blot、MTT和茜素红染色法分别测定对应组各指标变化情况。结果 ICR和E2一样能够明显提高成骨细胞ALP、OPG、OC和Runx2的表达,并能够显著降低RANKL和Dickkopf的表达,对应的OPG和RANKL蛋白的表达量与m RNA的表达量相一致。ALP活性、细胞增殖能力以及Ga2+结节数量与对照组相比也有明显提高。同时ICR和E2都能够有效回复DEX诱导的成骨抑制效应,这种调节效应能够被IN有效的阻断。结论 ICR具有促成骨细胞增殖分化和抑制破骨细胞激活效应,并能够有效的缓解DEX诱导的成骨抑制效应;其促成骨效应具ER依赖性。
Objective To investigate the effect of icariin (ICR) on osteogenic inhibition of MC3T3-E1 induced by estrogen receptor (ER) and dexamethasone (DEX). Methods The effects of DEX 10 5 mol·L -1, ICR 10 6 mol·L -1, estrogen 10 8 mol·L -1 and ICI 182780 (IN) 10 5 mol·L -1 MC3T3-E1 mature differentiation process, and the changes of each index of the corresponding group were determined by real-time RT-PCR, Westen blot, MTT and alizarin red staining. Results ICR, like E2, significantly increased the expression of ALP, OPG, OC and Runx2 in osteoblasts, and significantly reduced the expressions of RANKL and Dickkopf. The expression of OPG and RANKL corresponded with the expression of m RNA. ALP activity, cell proliferation and the number of Ga2 + nodules also increased significantly compared with the control group. At the same time, both ICR and E2 can effectively repress DEX-induced osteogenic inhibitory effect, which can be effectively blocked by IN. Conclusion ICR can promote the proliferation and differentiation of osteoblasts and inhibit the activation of osteoclasts, and can effectively relieve the osteogenic effect induced by DEX. The effect of ER on bone formation is ER-dependent.