Resveratrol prevents steroid-induced osteonecrosis of the femoral head via miR-146a modulation,Annals of the New York Academy of Sciences

当前位置： X-MOL 学术 › Ann. N. Y. Acad. Sci. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Resveratrol prevents steroid-induced osteonecrosis of the femoral head via miR-146a modulation
Annals of the New York Academy of Sciences ( IF 4.1 ) Pub Date : 2021-01-17 , DOI: 10.1111/nyas.14555
Kai Nan ₁ , Jun-Peng Pei ₂ , Li-Hong Fan ₁ , Yuan-Kai Zhang ₁ , Xin Zhang ₁ , Kang Liu ₃ , Zhi-Bin Shi ₁ , Xiao-Qian Dang ₁ , Kun-Zheng Wang ₁

Affiliation

The purpose of this study was to investigate the possible use of resveratrol (Res) to reverse abnormal osteogenesis/osteoclastogenesis activity that occurs during femoral head osteonecrosis and to explore the detailed mechanisms. Application of Res to bone marrow–derived mesenchymal stem cells in vitro promoted survival, inhibited apoptosis, and downregulated expression of reactive oxygen species expression. Moreover, Res application was associated with elevated microRNA-146a (miR-146a) expression, osteogenic differentiation, and suppressed osteoclastic differentiation, which were markedly reversed by miR-146a inhibitor. Histopathological observations and micro-computed tomography scanning results indicated that the Res-treated group had lower incidence of osteonecrosis and better bone microstructure than the untreated group. Res inhibited osteoclastogenesis through altering the levels of sirtuin1 (Sirt1), nuclear transcription factor-κB (NF-κB), and receptor activator of NF-κB ligand (RANKL). Simultaneously, Res treatment improved bone formation and increased β-catenin and runt-related transcription factor 2 (Runt2) expression levels, while reducing forkhead box class O (FOXO) family protein levels. The results of our study suggest that Res prevents steroid-induced osteonecrosis by upregulating miR-146a, and thereby stabilizes osteogenesis/osteoclastogenesis homeostasis via Wnt/FOXO and Sirt1/NF-κB pathways.

中文翻译：

白藜芦醇通过 miR-146a 调节预防类固醇诱导的股骨头坏死

本研究的目的是研究白藜芦醇 (Res) 可能用于逆转股骨头坏死期间发生的异常成骨/破骨细胞生成活动，并探讨其详细机制。Res在体外骨髓间充质干细胞中的应用促进存活，抑制细胞凋亡，并下调活性氧的表达。此外，Res 应用与升高的 microRNA-146a (miR-146a) 表达、成骨分化和抑制破骨细胞分化相关，这些都被 miR-146a 抑制剂显着逆转。组织病理学观察和显微计算机断层扫描结果表明，Res 治疗组的骨坏死发生率低于未治疗组，骨微观结构更好。Res 通过改变 Sirtuin1 (Sirt1)、核转录因子-κB (NF-κB) 和 NF-κB 配体受体激活剂 (RANKL) 的水平来抑制破骨细胞生成。同时，Res 治疗改善了骨形成并增加了 β-catenin 和 runt 相关转录因子 2 (Runt2) 的表达水平，同时降低叉头盒 O 类 (FOXO) 家族蛋白质水平。我们的研究结果表明，Res 通过上调 miR-146a 来预防类固醇诱导的骨坏死，从而通过 Wnt/FOXO 和 Sirt1/NF-κB 通路稳定成骨/破骨细胞生成稳态。

更新日期：2021-01-17

点击分享查看原文

点击收藏

阅读更多本刊最新论文本刊介绍/投稿指南11