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桃叶珊瑚苷抑制去卵巢小鼠破骨前体细胞融合并增强CD31/EMCN血管生成

Aucubin Impeded Preosteoclast Fusion and Enhanced CD31 EMCN Vessel Angiogenesis in Ovariectomized Mice.

作者信息

Li Ziyi, Liu Chang, Liu Xiaoli, Wang Na, Gao Liu, Bao Xiaoxue, Liu Sijing, Xue Peng

机构信息

Department of Endocrinology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China.

Key Orthopaedic Biomechanics Laboratory of Hebei Province, Shijiazhuang 050051, China.

出版信息

Stem Cells Int. 2022 Nov 9;2022:5226771. doi: 10.1155/2022/5226771. eCollection 2022.

DOI:10.1155/2022/5226771
PMID:36406003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9668463/
Abstract

Osteogenesis is tightly correlated with angiogenesis during the process of bone development, regeneration, and remodeling. In addition to providing nutrients and oxygen for bone tissue, blood vessels around bone tissue also secrete some factors to regulate bone formation. Type H vessels which were regulated by platelet-derived growth factor-BB (PDGF-BB) were confirmed to couple angiogenesis and osteogenesis. Recently, preosteoclasts have been identified as the most important source of PDGF-BB. Therefore, inhibiting osteoclast maturation, improving PDGF-BB secretion, stimulating type H angiogenesis, and subsequently accelerating bone regeneration may be potent treatments for bone loss disease. In the present study, aucubin, an iridoid glycoside extracted from and , was found to inhibit bone loss in ovariectomized mice. We further confirmed that aucubin could inhibit the fusion of tartrate-resistant acid phosphatase (TRAP) preosteoclasts into mature osteoclasts and indirectly increasing angiogenesis of type H vessel. The underlying mechanism is the aucubin-induced inhibition of MAPK/NF-B signaling, which increases the preosteoclast number and subsequently promotes angiogenesis via PDGF-BB. These results prompted that aucubin could be an antiosteoporosis drug candidate, which needs further research.

摘要

在骨骼发育、再生和重塑过程中,骨生成与血管生成密切相关。骨组织周围的血管除了为骨组织提供营养和氧气外,还分泌一些因子来调节骨形成。由血小板衍生生长因子-BB(PDGF-BB)调节的H型血管被证实可将血管生成与骨生成联系起来。最近,破骨细胞前体已被确定为PDGF-BB的最重要来源。因此,抑制破骨细胞成熟、改善PDGF-BB分泌、刺激H型血管生成并随后加速骨再生可能是治疗骨质流失疾病的有效方法。在本研究中,从[植物名称1]和[植物名称2]中提取的环烯醚萜苷类化合物桃叶珊瑚苷被发现可抑制去卵巢小鼠的骨质流失。我们进一步证实,桃叶珊瑚苷可抑制抗酒石酸酸性磷酸酶(TRAP)破骨细胞前体融合为成熟破骨细胞,并间接增加H型血管的血管生成。其潜在机制是桃叶珊瑚苷诱导的MAPK/NF-κB信号通路抑制,这增加了破骨细胞前体数量,并随后通过PDGF-BB促进血管生成。这些结果提示桃叶珊瑚苷可能是一种抗骨质疏松药物候选物,这需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/ddc49f296f9a/SCI2022-5226771.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/51731286a857/SCI2022-5226771.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/8cd30517e0a6/SCI2022-5226771.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/5d632fc7df00/SCI2022-5226771.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/78e3f65f95af/SCI2022-5226771.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/ab748ac44946/SCI2022-5226771.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/ddc49f296f9a/SCI2022-5226771.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/51731286a857/SCI2022-5226771.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/8cd30517e0a6/SCI2022-5226771.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/5d632fc7df00/SCI2022-5226771.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/78e3f65f95af/SCI2022-5226771.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/ab748ac44946/SCI2022-5226771.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eab8/9668463/ddc49f296f9a/SCI2022-5226771.006.jpg

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本文引用的文献

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Targeting actin-bundling protein L-plastin as an anabolic therapy for bone loss.靶向肌动蛋白结合蛋白 L-肌动蛋白作为治疗骨丢失的合成代谢疗法。
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Letrozole Suppresses the Fusion of Osteoclast Precursors through Inhibition of p38-Mediated DC-STAMP Pathway.
桃叶珊瑚苷对促进VEGFR2介导的血管生成和减少RANKL诱导的骨吸收的双重作用。
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promotes type H vessel formation and bone fracture healing by reducing gut permeability and inflammation.通过降低肠道通透性和炎症来促进 H 型血管形成和骨骨折愈合。
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