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骨间充质干细胞衍生的外泌体通过抑制氧化应激缓解压迫诱导的髓核细胞凋亡。

Exosomes Derived from Bone Mesenchymal Stem Cells Alleviate Compression-Induced Nucleus Pulposus Cell Apoptosis by Inhibiting Oxidative Stress.

机构信息

Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

出版信息

Oxid Med Cell Longev. 2021 Oct 25;2021:2310025. doi: 10.1155/2021/2310025. eCollection 2021.

DOI:10.1155/2021/2310025
PMID:34733401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8560283/
Abstract

Oxidative stress is relevant in compression-induced nucleus pulposus (NP) cell apoptosis and intervertebral disc (IVD) degeneration. Exosomes derived from bone mesenchymal stem cells (BMSCs-Exos) are key secretory products of MSCs, with important roles in tissue regeneration. This research is aimed at studying the protective impact of BMSCs-Exos on NP cell apoptosis caused by compression and investigating the underlying mechanisms. Our results indicated that we isolated BMSCs successfully. Exosomes were isolated from the BMSCs and found to alleviate the inhibitory effect that compression has on proliferation and viability in NP cells, decreasing the toxic effects of compression-induced NP cells. AnnexinV/PI double staining and TUNEL assays indicated that the BMSCs-Exos reduced compression-induced apoptosis. In addition, our research found that BMSCs-Exos suppressed compression-mediated NP oxidative stress by detecting the ROS and malondialdehyde level. Furthermore, BMSCs-Exos increased the mitochondrial membrane potential and alleviated compression-induced mitochondrial damage. These results indicate that BMSCs-Exos alleviate compression-mediated NP apoptosis by suppressing oxidative stress, which may provide a promising cell-free therapy for treating IVD degeneration.

摘要

氧化应激与压迫诱导的髓核细胞（NP）凋亡和椎间盘（IVD）退变有关。骨间充质干细胞（BMSCs-Exos）来源的外泌体是 MSC 的关键分泌产物，在组织再生中具有重要作用。本研究旨在研究 BMSCs-Exos 对压迫引起的 NP 细胞凋亡的保护作用，并探讨其潜在机制。我们的结果表明，我们成功分离了 BMSCs。从 BMSCs 中分离出外泌体，发现其可以减轻压迫对 NP 细胞增殖和活力的抑制作用，降低压迫诱导的 NP 细胞毒性作用。AnnexinV/PI 双染和 TUNEL 检测表明，BMSCs-Exos 减少了压迫诱导的细胞凋亡。此外，我们的研究发现，BMSCs-Exos 通过检测 ROS 和 MDA 水平抑制了压迫介导的 NP 氧化应激。此外，BMSCs-Exos 增加了线粒体膜电位，减轻了压迫诱导的线粒体损伤。这些结果表明，BMSCs-Exos 通过抑制氧化应激缓解压迫介导的 NP 细胞凋亡，为治疗 IVD 退变提供了一种有前途的无细胞治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/794faf479520/OMCL2021-2310025.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/d92074e5ca00/OMCL2021-2310025.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/a20648adddca/OMCL2021-2310025.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/6a958035f5ca/OMCL2021-2310025.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/a58230537115/OMCL2021-2310025.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/7b1dca351fc6/OMCL2021-2310025.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/794faf479520/OMCL2021-2310025.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/d92074e5ca00/OMCL2021-2310025.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/a20648adddca/OMCL2021-2310025.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/6a958035f5ca/OMCL2021-2310025.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/a58230537115/OMCL2021-2310025.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/7b1dca351fc6/OMCL2021-2310025.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aed/8560283/794faf479520/OMCL2021-2310025.006.jpg

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