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锶雷奈酸对 TGF-β1/BMP2 通路介导的兔激素性股骨头坏死的作用。

Effect of strontium ranelate on rabbits with steroid-induced osteonecrosis of femoral head through TGF-β1/BMP2 pathway.

机构信息

Joint Department of Orthopedics, 970 Hospital of the PLA JLSF, Yantai, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1000-1006. doi: 10.26355/eurrev_202002_20150.

Abstract

OBJECTIVE

To study the effect of strontium ranelate (SR) on steroid-induced osteonecrosis of the femoral head (SIONFH) in rabbits and its regulatory mechanism.

MATERIALS AND METHODS

The ONFH model was established in 30 rabbits using steroid and they were randomly divided into Control group, Model group, and SR group. After SR intervention, the rabbits were sacrificed and sampled. The pathological injury of the femoral head in each group was detected via hematoxylin-eosin (HE) staining, the level of vascular endothelial growth factor (VEGF) in the femoral head in each group was detected via enzyme-linked immunosorbent assay (ELISA). The messenger ribonucleic acid (mRNA) and protein expression levels of transforming growth factor-β1 (TGF-β1), as well as the bone morphogenetic protein 2 (BMP2) in the femoral head in each group, were determined using Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting.

RESULTS

The rabbit model of SIONFH was successfully established. Compared with Control group, the Model group had a severer pathological injury of the femoral head, a lower level of VEGF in the femoral head, significantly decreased mRNA and protein levels of TGF-β1 and BMP2. Compared with Model group, the SR group had markedly improved pathological injury of the femoral head, a higher level of VEGF in the femoral head, significantly increased mRNA and protein levels of TGF-β1, as well as BMP2.

CONCLUSIONS

SR can remarkably improve the pathological injury of the femoral head and increase the expression of VEGF in SIONFH rabbits, whose potential mechanism may be related to the activation of the TGF-β1/BMP2 signaling pathway.

摘要

目的

研究雷奈酸锶(SR)对兔激素性股骨头坏死(SIONFH)的作用及其调控机制。

材料与方法

30 只兔采用激素法建立 ONFH 模型,随机分为对照组、模型组和 SR 组。SR 干预后处死并取样。各组通过苏木精-伊红(HE)染色检测股骨头的病理损伤,酶联免疫吸附试验(ELISA)检测各组股骨头血管内皮生长因子(VEGF)水平。采用反转录-聚合酶链反应(RT-PCR)和 Western blot 检测各组股骨头转化生长因子-β1(TGF-β1)和骨形态发生蛋白 2(BMP2)的信使核糖核酸(mRNA)和蛋白表达水平。

结果

成功建立兔 SIONFH 模型。与对照组相比,模型组股骨头的病理损伤更严重,股骨头 VEGF 水平更低,TGF-β1 和 BMP2 的 mRNA 和蛋白表达水平显著降低。与模型组相比,SR 组股骨头的病理损伤明显改善,股骨头 VEGF 水平更高,TGF-β1 和 BMP2 的 mRNA 和蛋白表达水平显著增加。

结论

SR 可显著改善 SIONFH 兔的股骨头病理损伤,增加 VEGF 的表达,其潜在机制可能与 TGF-β1/BMP2 信号通路的激活有关。

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