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

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

Abstract

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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修饰黑磷量子点通过靶向AKT信号通路促进脊髓损伤修复。
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。
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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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