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修饰的黑磷量子点通过靶向AKT信号通路促进脊髓损伤修复。

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

作者信息

Xie Dong-Mei, Sun Chuanwei, Tu Qingqiang, Li Suyi, Zhang Yu, Mei Xifan, Li Yuanlong

机构信息

Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.

出版信息

J Tissue Eng. 2023 Jun 12;14:20417314231180033. doi: 10.1177/20417314231180033. eCollection 2023 Jan-Dec.

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.

摘要

脊髓损伤(SCI)是一种严重的中枢神经系统(CNS)难治性疾病,主要由高能创伤引起。现有的干预措施,如激素冲击和手术,都是不够理想的选择,这与继发性炎症和神经元功能障碍有关。具有神经保护作用的水凝胶引起了极大关注,本研究设计了一种包裹表没食子儿茶素-3-没食子酸酯(EGCG)的黑磷量子点(BPQDs)水凝胶(E@BP)用于炎症调节和脊髓损伤治疗。E@BP表现出良好的稳定性、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,并在体外增强神经元再生。此外,E@BP重建脊髓束的结构和功能完整性,促进移植后脊髓损伤大鼠运动神经元功能的恢复。重要的是,E@BP重启细胞周期并诱导神经再生。此外,E@BP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聚。事实上,E@BP调节神经再生和炎症反应的一个共同潜在机制是促进与AKT信号通路相关的关键蛋白的磷酸化。总之,E@BP可能通过减少炎症并通过AKT信号通路促进神经元再生来修复脊髓损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e02f/10272649/bb525d8db209/10.1177_20417314231180033-fig1.jpg

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