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丹酚酸B通过调节大鼠PPARγ表达预防激素性股骨头坏死

Salvianolic acid B prevents steroid-induced osteonecrosis of the femoral head via PPARγ expression in rats.

作者信息

Li Shuangqing, Wang Juan

机构信息

Department of Orthopedics, Cangzhou Central Hospital of Hebei, Cangzhou, Hebei 061001, P.R. China.

Department of Educational Administration, Cangzhou Medical College in Hebei, Cangzhou, Hebei 061001, P.R. China.

出版信息

Exp Ther Med. 2017 Feb;13(2):651-656. doi: 10.3892/etm.2016.4008. Epub 2016 Dec 28.

DOI:10.3892/etm.2016.4008
PMID:28352346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5348693/
Abstract

Salvianolic acid B (Sal B) is a water-soluble phenolic compound derived from . Recent studies show Sal B has a clear function of anti-cerebral ischemia injury, which is closely related to antioxidation, free radical scavenging, neuroprotection and the blood brain barrier. The aim of the present study was to verify whether Sal B prevents steroid-induced osteonecrosis of the femoral head and to investigate its underlying pharmacological mechanisms. Steroid-induced osteonecrosis rat models were established to evaluate the effects of Sal B on osteonecrotic changes and repair processes. The use of Sal B improved steroid-induced histopathological scores and inhibited osteoclast differentiation in rats. Notably, Sal B induced bone marrow-derived mesenchymal stem cells into osteogenesis. Moreover, Sal B treatment suppressed peroxisome proliferator-activated receptor (PPAR)γ and AP2 protein expression levels and increased runt-related transcription factor 2 and Collagen I protein expression levels in steroid-induced rats. osteocalcin and alkaline phosphatase content in steroid-induced rats was enhanced by treatment with Sal B. These results suggest that Sal B prevents steroid-induced osteonecrosis of the femoral head via PPARγ expression in rats. The present pilot study provides a brief insight into the effect of Sal B on steroid-induced osteonecrosis.

摘要

丹酚酸B(Sal B)是一种源自……的水溶性酚类化合物。最近的研究表明,丹酚酸B具有明确的抗脑缺血损伤功能,这与抗氧化、清除自由基、神经保护及血脑屏障密切相关。本研究的目的是验证丹酚酸B是否能预防类固醇诱导的股骨头坏死,并探究其潜在的药理机制。建立了类固醇诱导的股骨头坏死大鼠模型,以评估丹酚酸B对骨坏死变化和修复过程的影响。使用丹酚酸B可改善类固醇诱导的组织病理学评分,并抑制大鼠破骨细胞分化。值得注意的是,丹酚酸B能诱导骨髓间充质干细胞向成骨方向分化。此外,丹酚酸B处理可抑制类固醇诱导大鼠体内过氧化物酶体增殖物激活受体(PPAR)γ和AP2蛋白表达水平,并增加 runt相关转录因子2和I型胶原蛋白蛋白表达水平。丹酚酸B处理可提高类固醇诱导大鼠体内骨钙素和碱性磷酸酶含量。这些结果表明,丹酚酸B通过大鼠体内PPARγ表达预防类固醇诱导的股骨头坏死。本初步研究简要阐述了丹酚酸B对类固醇诱导的股骨头坏死的作用。

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