由MSC衍生的外体通过调节Keap1/Nrf2轴来改善椎间盘退化
Guangyu Xu1, Xiao Lu1, Siyang Liu1
1Department of Orthopedics, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Stem cell reviews and reports
|August 1, 2023
概括
骨髓介质干细胞衍生的外体细胞 (BMSC-exos) 减少骨髓介质干细胞退化 (IVDD) 中的氧化应激和炎症. 这些外体细胞通过调节Keap1/Nrf2通路来恢复抗氧化反应,减轻IVDD的进展.
科学领域:
- 再生医学是一种再生医学.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 椎间盘退化 (IVDD) 涉及由于减少Nrf2表达的反应性氧物种 (ROS) 的增加.
- 骨髓介质干细胞衍生的外体细胞 (BMSC-exos) 是细胞间通信的关键媒介,影响炎症,亡和组织修复.
研究的目的:
- 通过调节Keap1/Nrf2轴来研究BMSC-exos在减轻IVDD方面的治疗潜力.
- 阐明BMSC-exos在细胞核中减轻氧化应激和炎症的机制.
主要方法:
- 用BMSC-exos治疗退化的NP细胞和体内模型.
- 对Keap1,Nrf2,NF-κB表达和核转位的分析.
- 评估ROS产生,亡,炎症标志物和NP组织保留.
主要成果:
- 在NP细胞中,BMSC-exos抑制了Keap1并促进了Nrf2表达和核转位.
- 用BMSC-exos治疗减少了ROS的产生,亡和炎症.
- 在体内研究表明,在BMSC-exos治疗组中,NP组织保留和Nrf2和抗氧化蛋白的表达增加.
结论:
- 通过调节Keap1/Nrf2轴,BMSC-exos通过调节Keap1/Nrf2轴恢复退化的NP细胞中的抗氧化反应系统.
- 通过作为ROS调节器,BMSC-exos代表了IVDD的有希望的治疗策略.
- 通过Keap1/Nrf2通路,BMSC-exos通过减少氧化应激,炎症和亡来缓解IVDD.
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