Emodin enhances osteogenesis and inhibits adipogenesis.
Emodin enhances osteogenesis and inhibits adipogenesis.
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大黄素增强骨生成并抑制脂肪生成
DOI：
10.1186/1472-6882-14-74
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发表时间：
2014-02-24
影响因子：
--
通讯作者：
Lu ZM
中科院分区：
文献类型：
--
作者：
Yang F;Yuan PW;Hao YQ;Lu ZM
有研究表明，骨髓中成骨细胞的形成与脂肪形成密切相关，骨质疏松症中MSCs（间充质干细胞）的成骨和脂肪分化之间的平衡被破坏。为了改善骨质疏松症的治疗，迫切需要具有调节平衡作用的药物。大黄素是一种从中草药中提取的天然蒽醌衍生物，几千年来一直用于治疗骨病。然而，大黄素调节成骨和脂肪形成的潜在分子机制仍然知之甚少。研究了大黄素对去卵巢小鼠和骨髓间充质干细胞成骨和脂肪生成过程的分子机制。分析了大黄素在体内和体外的作用。雌性ICR小鼠分为3组：假手术组、卵巢切除组、大黄素组。采用H&E、免疫组化、Micro-CT评价疗效。体外实验采用ALP、油红O染色、实时RT-PCR和western blot等方法分析0.1 μM ~ 10 μM浓度的大黄素对BMSCs诱导成骨和抑制脂肪生成过程的影响。我们的实验表明，大黄素可以增加成骨细胞数量、骨密度、骨小梁体积分数（BV/TV）、Tb。N（小梁数）和Conn.D（连通性密度），减少骨髓脂肪组织和脂肪细胞。成骨标志物Runx2、osterix、I型胶原、骨钙素、ALP等基因和蛋白表达上调。与脂肪形成相关的基因和蛋白、PPARγ、C/EBPα和ap2均下调。证明大黄素抑制脂肪细胞分化，促进骨髓间充质干细胞向成骨细胞分化。
It has been suggested that the formation of osteoblasts in bone marrow is closely associated with adipogenesis, and the balance between osteogenesis and adipogenesis differentiation of MSCs (mesenchymal stem cells) is disrupted in osteoporosis. In order to improve the treatment of osteoporosis, available agents with roles of regulating the balance is highly desirable. Emodin is a natural anthraquinone derivative extracted from Chinese herbs, which have been used to treat bone diseases for thousands of years. However, the underlying molecular mechanisms of emodin in modulating osteogenesis and adipogenesis remain poorly understood. The molecular mechanisms of emodin on the processes of osteogenesis and adipogenesis in ovariectomized mouse and BMSCs (bone marrow mesenchymal stem cells) have been studied. We have analyzed the effects of emodin in vivo and in vitro. Female ICR mice were assigned to three groups: sham group, ovariectomy group, emodin group. Efficacy was evaluated by H&E, immunohistochemical assay and Micro-CT. In vitro, we analyze the effect of emodin—at concentrations between 0.1 μM and 10 μM-on the processes of inducing osteogenesis and inhibiting adipogenesis in BMSCs by ALP, Oil red O staining, real time RT-PCR and western blot. As our experiment shows that emodin could increase the number of osteoblast, BMD (bone mineral density), BV/TV (trabecular bone volume fraction), Tb.N (trabecular number) and Conn.D (connectivity density) of OVX (ovariectomized) mice and decrease the bone marrow fat tissue and adipocytes. The genes and proteins expression of osteogenesis markers, such as Runx2, osterix, collagen type I, osteocalcin, or ALP were up-regulated. While, the genes and proteins involved in adipogenesis, PPARγ, C/EBPα and ap2 were down-regulated. It proves that emodin inhibits adipocyte differentiation and enhances osteoblast differentiation from BMSCs.
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