Dong Li, Chenhao Cao, Zhuofan Li, Zhiyong Chang, Ping Cai, Chenxi Zhou, Jun Liu, Kaihua Li, Bin Du
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引用次数: 0
摘要
淫羊藿苷 II 是一种黄酮苷，是服用附子草后在体内发现的主要成分，具有一些药理作用，如预防骨质疏松症和增强免疫力。骨髓脂肪组织水平的增加与骨质疏松症有关。S100 钙结合蛋白 A16（S100A16）可促进骨髓间充质干细胞分化为脂肪细胞。本研究旨在通过抑制S100A16的表达来证实淫羊藿苷II在骨髓中抗脂肪生成的作用。我们使用了卵巢切除术（OVX）和骨髓干细胞模型。结果表明，淫羊藿苷II能降低骨髓脂肪含量，抑制骨髓造血干细胞的成脂分化和S100A16的表达，而S100A16的表达与脂肪生成有关。过表达S100A16可消除淫羊藿苷II对脂肪形成的抑制作用。β-catenin参与调节骨中淫羊藿苷II/S100A16介导的脂肪生成。总之，淫羊藿苷II通过下调S100A16保护OVX诱导的骨髓脂肪生成，β-catenin可能也参与其中。
Icariside II protects from marrow adipose tissue (MAT) expansion in estrogen-deficient mice by targeting S100A16.
Icariside II, a flavonoid glycoside, is the main component found invivo after the administration of Herba epimedii and has shown some pharmacological effects, such as prevention of osteoporosis and enhancement of immunity. Increased levels of marrow adipose tissue are associated with osteoporosis. S100 calcium-binding protein A16 (S100A16) promotes the differentiation of bone marrow mesenchymal stem cells (BMSCs) into adipocytes. This study aimed to confirm the anti-lipidogenesis effect of Icariside II in the bone marrow by inhibiting S100A16 expression. We used ovariectomy (OVX) and BMSC models. The results showed that Icariside II reduced bone marrow fat content and inhibited BMSCs adipogenic differentiation and S100A16 expression, which correlated with lipogenesis. Overexpression of S100A16 eliminated the inhibitory effect of Icariside II on lipid formation. β-catenin participated in the regulation adipogenesis mediated by Icariside II/S100A16 in the bone. In conclusion, Icariside II protects against OVX-induced bone marrow adipogenesis by downregulating S100A16, in which β-catenin might also be involved.
期刊介绍：
The Journal of Molecular Endocrinology is an official journal of the Society for Endocrinology and is endorsed by the European Society of Endocrinology and the Endocrine Society of Australia.
Journal of Molecular Endocrinology is a leading global journal that publishes original research articles and reviews. The journal focuses on molecular and cellular mechanisms in endocrinology, including: gene regulation, cell biology, signalling, mutations, transgenics, hormone-dependant cancers, nuclear receptors, and omics. Basic and pathophysiological studies at the molecule and cell level are considered, as well as human sample studies where this is the experimental model of choice. Technique studies including CRISPR or gene editing are also encouraged.
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