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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >The Combination of Adipose-derived Schwann-like Cells and Acellular Nerve Allografts Promotes Sciatic Nerve Regeneration and Repair through the JAK2/STAT3 Signaling Pathway in Rats
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The Combination of Adipose-derived Schwann-like Cells and Acellular Nerve Allografts Promotes Sciatic Nerve Regeneration and Repair through the JAK2/STAT3 Signaling Pathway in Rats

机译:脂肪衍生的施曼样细胞和细胞神经异种移植物的组合促进了坐骨神经再生和通过大鼠的JAK2 / Stat3信号传导途径修复

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Schwann cells (SCs) combined with acellular nerve allografts (ANAs) effectively promote the regeneration and repair of peripheral nerves, but the exact mechanism has not been fully elucidated. However, the disadvantages of SCs include their limited source and slow rate of expansion in vitro. Previous studies have found that adipose-derived stem cells have the ability to differentiate into Schwann-like cells. Therefore, we speculated that Schwann-like cells combined with ANAs could profoundly facilitate nerve regeneration and repair. The aim of the present study was to investigate the cellular and molecular mechanisms of regeneration and repair. In this study, tissue-engineered nerves were first constructed by adipose-derived Schwann-like cells and ANAs to bridge missing sciatic nerves. Then, the rats were randomly divided into five groups (n = 12 per group): a Control group; a Model group; an ADSC group; an SC-L group; and a DMEM group. Twelve weeks postsurgery, behavioral function tests and molecular biological techniques were used to evaluate the function of regenerated nerves and the relevant molecular mechanisms after sciatic nerve injury (SNI). The results showed that adipose-derived Schwann-like cells combined with ANAs markedly promoted sciatic nerve regeneration and repair. These findings also demonstrated that the expression of neurotrophic factors (NFs) was increased, and the expression of Janus activated kinase2 (JAK2)/P-JAK2, signal transducer and activator of transcription-3 (STAT3)/P-STAT3 was decreased in the spinal cord after SNI. Therefore, these results suggested that highly expressed NFs in the spinal cord could promote nerve regeneration and repair by inhibiting activation of the JAK2/STAT3 signaling pathway. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.
机译:Schwann细胞(SCS)与细胞神经同种异体移植物(ANAS)相结合,有效地促进了外周神经的再生和修复,但确切的机制尚未完全阐明。然而,SCS的缺点包括它们的有限源和体外膨胀速率。以前的研究发现,脂肪衍生的干细胞具有区分施旺的细胞的能力。因此,我们推测施旺的细胞与ANA相结合,可以深刻促进神经再生和修复。本研究的目的是探讨再生和修复的细胞和分子机制。在该研究中,首先通过脂肪衍生的施曼样细胞和肛门构建组织工程神经,以弥合缺少坐骨神经。然后,将大鼠随机分为五组(每组n = 12):对照组;模型组; ADSC组; SC-L集团;和一个DMEM组。第十四周后期,行为函数试验和分子生物技术用于评估再生神经的功能和坐骨神经损伤(SNI)后的相关分子机制。结果表明,脂肪衍生的施曼样细胞与ANAS相结合明显促进坐骨神经再生和修复。这些发现还证明了神经营养因子(NFS)的表达增加,并且Janus活化激酶2(JAK2)/ p-JAK2,信号传感器和转录-3(STAT3)/ P-STAT3的活化剂的表达减少脊柱脊髓。因此,这些结果表明,脊髓中高表达的NFS可以通过抑制JAK2 / Stat3信号传导途径的激活来促进神经再生和修复。 (c)2019年IBRO。 elsevier有限公司出版。保留所有权利。

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