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表没食子儿茶素-3-没食子酸酯可保护人骨髓间充质干细胞免受过氧化氢诱导的成骨分化抑制。

Epigallocatechin-3-gallate Protects against Hydrogen Peroxide-Induced Inhibition of Osteogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells.

作者信息

Wang Dawei, Wang Yonghui, Xu Shihong, Wang Fu, Wang Bomin, Han Ke, Sun Daqing, Li Lianxin

机构信息

Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.

Department of Vascular Surgery, Second Hospital of Shandong University, Jinan 250000, China.

出版信息

Stem Cells Int. 2016;2016:7532798. doi: 10.1155/2016/7532798. Epub 2016 Feb 9.

Abstract

Oxidative stress induces bone loss and osteoporosis, and epigallocatechin-3-gallate (EGCG) may be used to combat these diseases due to its antioxidative property. Herein, oxidative stress in human bone marrow-derived mesenchymal stem cells (BM-MSCs) was induced by H2O2, resulting in an adverse effect on their osteogenic differentiation. However, this H2O2-induced adverse effect was nullified when the cells were treated with EGCG. In addition, treatment of BM-MSCs with EGCG alone also resulted in the enhancement of osteogenic differentiation of BM-MSCs. After EGCG treatment, expressions of β-catenin and cyclin D1 were upregulated, suggesting that the Wnt pathway was involved in the effects of EGCG on the osteogenic differentiation of BM-MSCs. This was also confirmed by the fact that the Wnt pathway inhibitor, Dickkopf-1 (DKK-1), can nullify the EGCG-induced enhancement effect on BM-MSC's osteogenic differentiation. Hence, our results suggested that EGCG can reduce the effects of oxidative stress on Wnt pathway in osteogenic cells, which supported a potentially promising therapy of bone disorders induced by oxidative stress. Considering its positive effects on BM-MSCs, EGCG may also be beneficial for stem cell-based bone repair.

摘要

氧化应激会导致骨质流失和骨质疏松,而表没食子儿茶素-3-没食子酸酯(EGCG)因其抗氧化特性可用于对抗这些疾病。在此,过氧化氢(H2O2)诱导了人骨髓间充质干细胞(BM-MSCs)中的氧化应激,对其成骨分化产生了不利影响。然而,当用EGCG处理细胞时,这种H2O2诱导的不利影响被消除了。此外,单独用EGCG处理BM-MSCs也导致其成骨分化增强。EGCG处理后,β-连环蛋白和细胞周期蛋白D1的表达上调,表明Wnt信号通路参与了EGCG对BM-MSCs成骨分化的影响。Wnt信号通路抑制剂Dickkopf-1(DKK-1)能够消除EGCG诱导的BM-MSCs成骨分化增强效应,这一事实也证实了这一点。因此,我们的结果表明,EGCG可以减少氧化应激对成骨细胞中Wnt信号通路的影响,这为氧化应激诱导的骨疾病提供了一种潜在的有前景的治疗方法。考虑到其对BM-MSCs的积极作用,EGCG可能对基于干细胞的骨修复也有益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06e4/4763004/1bd98004c99f/SCI2016-7532798.001.jpg

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