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二氢杨梅素通过调控骨硬化蛋白表达促进骨髓间充质干细胞成骨分化。

Icaritin promotes the osteogenesis of bone marrow mesenchymal stem cells via the regulation of sclerostin expression.

机构信息

Hip Preserving Ward, No. 3 Orthopedic Region, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510407, P.R. China.

Department of Orthopedics, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260, P.R. China.

出版信息

Int J Mol Med. 2020 Mar;45(3):816-824. doi: 10.3892/ijmm.2020.4470. Epub 2020 Jan 20.

DOI:10.3892/ijmm.2020.4470
PMID:31985018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7015123/
Abstract

Icaritin, a metabolite of icariin, is a potent promoter of bone marrow‑derived mesenchymal stem cells (BMSCs) osteogenesis, but the underlying mechanisms remain unclear. To examine the effects of icaritin on osteogenic differentiation, BMSCs were exposed to osteogenic induction medium with or without icaritin pretreatment in the present study. It was identified that icaritin (0.01‑1 µM) exhibited no cytotoxicity on the proliferative abilities of the BMSCs. Icaritin at 1 µM increased alkaline phosphatase activity, mineral deposition and osteoblast‑specific gene expression. Treatment with 1 µM Icaritin upregulated osteocalcin, RUNX family transcription factor 2, tissue‑nonspecific alkaline phosphatase and β‑catenin, and suppressed sclerostin (SOST) gene expression in different stages of osteogenic differentiation. It was also demonstrated that SOST overexpression inhibited icaritin‑induced osteogenesis. The western blot analysis data suggested that ICI 182780, which causes estrogen receptor α (ERα) degradation, reversed the icaritin‑induced decrease in SOST expression, which was inconsistent with the results of immunofluorescence analysis. In conclusion, icaritin was demonstrated to promote the osteogenesis of hBMSCs by downregulating SOST expression, and icaritin‑induced suppression of SOST was regulated in part via the Wnt/β‑catenin/ERα axis.

摘要

朝藿定 C，淫羊藿素的一种代谢产物，是骨髓间充质干细胞（BMSCs）成骨的有效促进剂，但作用机制尚不清楚。本研究旨在探讨朝藿定 C 对成骨分化的影响，将 BMSCs 分别用或不用朝藿定 C 预处理后置于成骨诱导培养基中。结果表明，朝藿定 C（0.01-1 μM）对 BMSCs 的增殖能力无细胞毒性。1 μM 朝藿定 C 增加碱性磷酸酶活性、矿化沉积和成骨特异性基因表达。用 1 μM 朝藿定 C 处理可上调不同成骨分化阶段的骨钙素、RUNX 家族转录因子 2、组织非特异性碱性磷酸酶和β-连环蛋白的表达，并抑制骨硬化蛋白（SOST）基因的表达。实验还证明，SOST 过表达抑制了朝藿定 C 诱导的成骨作用。Western blot 分析数据表明，导致雌激素受体 α（ERα）降解的 ICI 182780 逆转了朝藿定 C 诱导的 SOST 表达下降，这与免疫荧光分析的结果不一致。综上所述，朝藿定 C 通过下调 SOST 表达促进 hBMSCs 的成骨作用，朝藿定 C 诱导的 SOST 抑制部分通过 Wnt/β-连环蛋白/ERα 轴调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/8bec44fa84b2/IJMM-45-03-0816-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/3c0267509bcd/IJMM-45-03-0816-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/1feb2be022a5/IJMM-45-03-0816-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/d3851e2e7e5a/IJMM-45-03-0816-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/4d104b5fff47/IJMM-45-03-0816-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/5482968f892c/IJMM-45-03-0816-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/a93cc7ae41c7/IJMM-45-03-0816-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/6d6ae816b1ce/IJMM-45-03-0816-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/8bec44fa84b2/IJMM-45-03-0816-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/3c0267509bcd/IJMM-45-03-0816-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/1feb2be022a5/IJMM-45-03-0816-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/d3851e2e7e5a/IJMM-45-03-0816-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/4d104b5fff47/IJMM-45-03-0816-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/5482968f892c/IJMM-45-03-0816-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/a93cc7ae41c7/IJMM-45-03-0816-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/6d6ae816b1ce/IJMM-45-03-0816-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7f4/7015123/8bec44fa84b2/IJMM-45-03-0816-g07.jpg

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