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阿萨皂素 VI 通过骨质疏松症模型中的 PI3K/AKT 信号通路促进骨髓基质细胞成骨分化。

Asperosaponin VI promotes bone marrow stromal cell osteogenic differentiation through the PI3K/AKT signaling pathway in an osteoporosis model.

机构信息

Hangzhou Medical College Binwen Road,Hangzhou,310053, China.

Stomatology Hospital, School of Medicine, Zhejiang university, Yan'an Road, Hangzhou 310006, China.

出版信息

Sci Rep. 2016 Oct 19;6:35233. doi: 10.1038/srep35233.

DOI:10.1038/srep35233
PMID:27756897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5069473/
Abstract

Asperosaponin VI (ASA VI), a natural compound isolated from the well-known traditional Chinese herb Radix Dipsaci, has an important role in promoting osteoblast formation. However, its effects on osteoblasts in the context of osteoporosis is unknown. This study aimed to investigate the effects and mechanism of ASA VI action on the proliferation and osteogenic differentiation of bone marrow stromal cells isolated from the ovariectomized rats (OVX rBMSCs). The toxicity of ASA VI and its effects on the proliferation of OVX rBMSCs were measured using a CCK-8 assay. Various osteogenic differentiation markers were also analyzed, such as ALP activity, calcified nodule formation, and the expression of osteogenic genes, i.e., ALP, OCN, COL 1 and RUNX2. The results indicated that ASA VI promoted the proliferation of OVX rBMSCs and enhanced ALP activity and calcified nodule formation. In addition, while ASA VI enhanced the expression of ALP, OCN, Col 1 and RUNX2, treatment with LY294002 reduced all of these osteogenic effects and reduced the p-AKT levels induced by ASA VI. These results suggest that ASA VI promotes the osteogenic differentiation of OVX rBMSCs by acting on the phosphatidylinositol-3 kinase/AKT signaling pathway.

摘要

薯蓣皂苷 VI(ASA VI)是从著名的传统中药续断中分离得到的一种天然化合物,在促进成骨细胞形成方面具有重要作用。然而,其在骨质疏松症背景下对成骨细胞的作用尚不清楚。本研究旨在探讨 ASA VI 对去卵巢大鼠骨髓基质细胞(OVX rBMSCs)增殖和成骨分化的作用及其机制。采用 CCK-8 法测定 ASA VI 的毒性及其对 OVX rBMSCs 增殖的影响。分析了各种成骨分化标志物,如碱性磷酸酶(ALP)活性、钙化结节形成以及成骨基因(如 ALP、OCN、COL 1 和 RUNX2)的表达。结果表明,ASA VI 促进了 OVX rBMSCs 的增殖,增强了 ALP 活性和钙化结节形成。此外,虽然 ASA VI 增强了 ALP、OCN、Col 1 和 RUNX2 的表达,但 LY294002 处理降低了所有这些成骨作用,并降低了 ASA VI 诱导的 p-AKT 水平。这些结果表明,ASA VI 通过作用于磷脂酰肌醇-3 激酶/AKT 信号通路促进 OVX rBMSCs 的成骨分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/96e609727dd5/srep35233-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/ac8abc085bee/srep35233-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/94049571e6f2/srep35233-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/423f822f85e6/srep35233-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/4f1b05d0cc0c/srep35233-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/bd3735f77034/srep35233-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/96e609727dd5/srep35233-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/ac8abc085bee/srep35233-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/94049571e6f2/srep35233-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/423f822f85e6/srep35233-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/4f1b05d0cc0c/srep35233-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/bd3735f77034/srep35233-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/5069473/96e609727dd5/srep35233-f6.jpg

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