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骨髓间充质干细胞通过 Nrf2 通路对抗氧化应激损伤的新策略:氧化应激预处理。

New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning.

机构信息

Department of Trauma orthopedics, The Affliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.

Trauma Teaching and Research Department, Guizhou Medical University, Guiyang, Guizhou, China.

出版信息

J Cell Biochem. 2019 Dec;120(12):19902-19914. doi: 10.1002/jcb.29298. Epub 2019 Jul 26.

Abstract

Clinically, bone marrow mesenchymal stem cells (BMSCs) have been used in treatment of many diseases, but the local oxidative stress (OS) of lesion severely limits the survival of BMSCs, which reduces the efficacy of BMSCs transplantation. Therefore, enhancing the anti-OS stress ability of BMSCs is a key breakthrough point. Preconditioning is a common protective mechanism for cells or body. Here, the aim of this study was to investigate the effects of OS preconditioning on the anti-OS ability of BMSCs and its mechanism. Fortunately, OS preconditioning can increase the expression of superoxide dismutase, catalase, NQO1, and heme oxygenase 1 through the nuclear factor erythroid 2-related factor 2 pathway, thereby decreased the intracellular reactive oxygen species (ROS) levels, relieved the damage of ROS to mitochondria, DNA and cell membrane, enhanced the anti-OS ability of BMSCs, and promoted the survival of BMSCs under OS.

摘要

临床上,骨髓间充质干细胞(BMSCs)已被用于治疗许多疾病,但病变部位的局部氧化应激(OS)严重限制了 BMSCs 的存活,从而降低了 BMSCs 移植的疗效。因此,增强 BMSCs 的抗 OS 应激能力是一个关键的突破点。预处理是细胞或机体的一种常见保护机制。本研究旨在探讨 OS 预处理对 BMSCs 抗 OS 能力的影响及其机制。幸运的是,OS 预处理可以通过核因子红细胞 2 相关因子 2 通路增加超氧化物歧化酶、过氧化氢酶、NQO1 和血红素加氧酶 1 的表达,从而降低细胞内活性氧(ROS)水平,减轻 ROS 对线粒体、DNA 和细胞膜的损伤,增强 BMSCs 的抗 OS 能力,并促进 BMSCs 在 OS 下的存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d982/6852471/5a0713dd2e98/JCB-120-19902-g001.jpg

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