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朝藿定黄酮通过抑制成骨细胞和破骨细胞的凋亡来预防糖皮质激素诱导的骨质疏松症。

Alpinumisoflavone protects against glucocorticoid-induced osteoporosis through suppressing the apoptosis of osteoblastic and osteocytic cells.

机构信息

Department of Orthopedics, Ningbo No. 2 Hospital, Ningbo, 315104, China.

Department of Human Morphology, Ningbo College of Health Science, No. 51 Xuefu Road, Ningbo, Zhejiang, 315104, China.

出版信息

Biomed Pharmacother. 2017 Dec;96:993-999. doi: 10.1016/j.biopha.2017.11.136. Epub 2017 Dec 6.

DOI:10.1016/j.biopha.2017.11.136
PMID:29203387
Abstract

The long-term use of glucocorticoids is found to cause osteoporosis. This study is designed to evaluate the protective effect of alpinumisoflavone (AIF), a naturally occurring flavonoid compound, on dexamethasone(Dex)-induced osteoporosis. We use a rat model to investigate the apoptosis of osteoblastic and osteocytic cells. The results indicate that AIF effectively protects against dexamethasone-induced osteoporosis. Moreover, AIF effectively reversed dexamethasone-induced apoptosis in osteoblastic and osteocytic cells through inhibiting ROS overproduction and regulating the Nrf2 pathway. In conclusion, the AIF activated Nrf2 signaling pathway was observed to suppress Dex-induced ROS production in osteoblastic and osteocytic cells, which may explain its anti-osteoporotic effects against dexamethasone-induced osteoporosis.

摘要

长期使用糖皮质激素会导致骨质疏松。本研究旨在评估一种天然存在的黄酮类化合物阿尔卑斯山大豆异黄酮(AIF)对地塞米松(Dex)诱导的骨质疏松症的保护作用。我们使用大鼠模型来研究成骨细胞和破骨细胞的凋亡。结果表明,AIF 能有效防治地塞米松诱导的骨质疏松症。此外,AIF 通过抑制 ROS 的过度产生和调节 Nrf2 通路,有效地逆转了地塞米松诱导的成骨细胞和破骨细胞凋亡。总之,观察到 AIF 激活的 Nrf2 信号通路抑制了成骨细胞和破骨细胞中 Dex 诱导的 ROS 产生,这可能解释了其对地塞米松诱导的骨质疏松症的抗骨质疏松作用。

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