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泼尼松龙诱导斑马鱼幼鱼骨质疏松症的可能机制。

Possible mechanisms of prednisolone-induced osteoporosis in zebrafish larva.

机构信息

Department of Orthopaedics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China.

Department of Orthopaedics, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.

出版信息

Biomed Pharmacother. 2018 May;101:981-987. doi: 10.1016/j.biopha.2018.02.082. Epub 2018 Mar 22.

Abstract

Glucocorticoid-induced osteoporosis (GIOP) is a serious clinical bone disease that results from the long-term consumption of glucocorticoids or glucocorticoid-like drugs. Although many studies have attempted to determine the mechanisms of GIOP, they are still unclear. In this study, we established a zebrafish model of glucocorticoid-like drug-induced osteoporosis by treating larvae with prednisolone. We then quantified the expression of a selection of extracellular matrix (ECM)-, osteoblast-, and osteoclast-related genes. Our results showed that at 15 days post fertilization, zebrafish larvae treated with 25 μM prednisolone are a suitable model for GIOP, not only owing to the decrease in robust bone mass but also because of significant alterations in gene expression. The quantification of the expression of ECM-, osteoblast-, and osteoclast- related genes revealed that mmp9 and mmp13 were significantly upregulated and entpd5a, acp5a, and sost were significantly downregulated. These genes may be a target for future research into GIOP. Our study thus provides new insights into GIOP.

摘要

糖皮质激素诱导性骨质疏松症(GIOP)是一种严重的临床骨疾病,由长期使用糖皮质激素或类皮质激素药物引起。尽管许多研究试图确定 GIOP 的机制,但仍不清楚。在这项研究中,我们通过用泼尼松龙处理幼虫,建立了糖皮质激素样药物诱导的骨质疏松症的斑马鱼模型。然后,我们定量了选择的细胞外基质(ECM)、成骨细胞和破骨细胞相关基因的表达。我们的结果表明,在受精后 15 天,用 25μM 泼尼松龙处理的斑马鱼幼虫是 GIOP 的合适模型,不仅由于坚固的骨量减少,而且由于基因表达的显著改变。ECM、成骨细胞和破骨细胞相关基因表达的定量显示,mmp9 和 mmp13 显著上调,而 entpd5a、acp5a 和 sost 显著下调。这些基因可能是未来 GIOP 研究的靶点。因此,我们的研究为 GIOP 提供了新的见解。

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