修饰黑磷量子点通过靶向AKT信号通路促进脊髓损伤修复。

IF 6.7 1区 工程技术 Q1 CELL & TISSUE ENGINEERING
Dong-Mei Xie, Chuanwei Sun, Qingqiang Tu, Suyi Li, Yu Zhang, Xifan Mei, Yuanlong Li
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引用次数: 2

摘要

脊髓损伤(SCI)是一种严重的中枢神经系统(CNS)顽固性疾病,多由高能创伤引起。现有的干预措施,如激素休克和手术是不够的选择,这涉及到继发性炎症和神经功能障碍。具有神经元保护作用的水凝胶引起了人们的极大关注,本研究设计了包封表没食子儿茶素-3-没食子酸酯(EGCG)水凝胶的黑磷量子点(BPQDs) (E@BP)用于炎症调节和脊髓损伤治疗。E@BP具有良好的稳定性、生物相容性和安全性。E@BP孵育可减轻脂多糖(LPS)诱导的原代神经元炎症,增强体外神经元再生。此外,E@BP重建脊髓束结构和功能的完整性,促进脊髓损伤大鼠移植后运动神经元功能的恢复。重要的是,E@BP重新启动细胞周期并诱导神经再生。此外,E@BP可减轻脊髓损伤组织的局部炎症,其特征是减少星形胶质细胞、小胶质细胞、巨噬细胞和少突胶质细胞的积累。事实上,E@BP调节神经再生和炎症反应的共同潜在机制是促进AKT信号通路相关关键蛋白的磷酸化。总之,E@BP可能通过AKT信号通路减少炎症和促进神经元再生来修复脊髓损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway.

Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway.

Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway.

Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway.

Spinal cord injury (SCI) is a serious refractory disease of the central nervous system (CNS), which mostly caused by high-energy trauma. Existing interventions such as hormone shock and surgery are insufficient options, which relate to the secondary inflammation and neuronal dysfunction. Hydrogel with neuron-protective behaviors attracts tremendous attention, and black phosphorus quantum dots (BPQDs) encapsulating with Epigallocatechin-3-gallate (EGCG) hydrogels (E@BP) is designed for inflammatory modulation and SCI treatment in this study. E@BP displays good stability, biocompatibility and safety profiles. E@BP incubation alleviates lipopolysaccharide (LPS)-induced inflammation of primary neurons and enhances neuronal regeneration in vitro. Furthermore, E@BP reconstructs structural versus functional integrity of spinal cord tracts, which promotes recovery of motor neuron function in SCI rats after transplantation. Importantly, E@BP restarts the cell cycle and induces nerve regeneration. Moreover, E@BP diminishes local inflammation of SCI tissues, characterized by reducing accumulation of astrocyte, microglia, macrophages, and oligodendrocytes. Indeed, a common underlying mechanism of E@BP regulating neural regenerative and inflammatory responses is to promote the phosphorylation of key proteins related to AKT signaling pathway. Together, E@BP probably repairs SCI by reducing inflammation and promoting neuronal regeneration via the AKT signaling pathway.

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来源期刊
Journal of Tissue Engineering
Journal of Tissue Engineering Engineering-Biomedical Engineering
CiteScore
11.60
自引率
4.90%
发文量
52
审稿时长
12 weeks
期刊介绍: The Journal of Tissue Engineering (JTE) is a peer-reviewed, open-access journal dedicated to scientific research in the field of tissue engineering and its clinical applications. Our journal encompasses a wide range of interests, from the fundamental aspects of stem cells and progenitor cells, including their expansion to viable numbers, to an in-depth understanding of their differentiation processes. Join us in exploring the latest advancements in tissue engineering and its clinical translation.
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