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骨髓基质细胞部分通过Toll样受体4/核因子κB信号通路改善脊髓损伤大鼠的功能恢复。

Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll-like receptor-4/nuclear factor-κB signaling pathway.

作者信息

Bai Shi, Zhou Hao, Wu Lijuan

机构信息

Department of Anatomy, School of Medicine, Taizhou University, Taizhou, Zhejiang 317000, P.R. China.

School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.

出版信息

Exp Ther Med. 2019 Jan;17(1):444-448. doi: 10.3892/etm.2018.6907. Epub 2018 Oct 31.

Abstract

Spinal cord injury (SCI) results in inflammation, and TLR4, which is an inflammatory factor, has an important role in the pathological injury that occurs following SCI. Recently, bone marrow stromal cells (BMSCs) have been demonstrated to be a novel treatment in SCI. However, the underlying mechanism of neuroprotection in SCI by BMSCs remains unclear. The present study was designed to investigate the therapeutic mechanism of BMSCs in SCI by analysis of Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) expression. The present results demonstrated that BMSC transplantation promoted functional recovery and tissue repair in SCI rats. Interestingly, it also reduced the expression of TLR4 and NF-κB after SCI. Furthermore, it was demonstrated that BMSCs downregulated the expression of apoptosis factor caspase-12 in the SCI rat model. The present results demonstrated that BMSCs may have incorporated into the spinal cord to improve locomotor function after SCI, partly via the TLR4/NF-κB signaling pathway. To the best of our knowledge, this is the first study to determine that BMSCs prevented secondary injury and enhanced functional recovery in SCI via inhibition of TLR4/NF-κB-mediated inflammation.

摘要

脊髓损伤(SCI)会引发炎症,而作为一种炎症因子的Toll样受体4(TLR4)在SCI后发生的病理损伤中起重要作用。最近,骨髓基质细胞(BMSCs)已被证明是SCI的一种新型治疗方法。然而,BMSCs对SCI神经保护的潜在机制仍不清楚。本研究旨在通过分析Toll样受体4(TLR4)/核因子-κB(NF-κB)的表达来探讨BMSCs在SCI中的治疗机制。目前的结果表明,BMSC移植促进了SCI大鼠的功能恢复和组织修复。有趣的是,它还降低了SCI后TLR4和NF-κB的表达。此外,在SCI大鼠模型中证明BMSCs下调了凋亡因子caspase-12的表达。目前的结果表明,BMSCs可能已融入脊髓以改善SCI后的运动功能,部分是通过TLR4/NF-κB信号通路。据我们所知,这是第一项确定BMSCs通过抑制TLR4/NF-κB介导的炎症预防SCI继发性损伤并增强功能恢复的研究。

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