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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 wi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272649/ https://www.ncbi.nlm.nih.gov/pubmed/37333896 http://dx.doi.org/10.1177/20417314231180033 |
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author | Xie, Dong-Mei Sun, Chuanwei Tu, Qingqiang Li, Suyi Zhang, Yu Mei, Xifan Li, Yuanlong |
author_facet | Xie, Dong-Mei Sun, Chuanwei Tu, Qingqiang Li, Suyi Zhang, Yu Mei, Xifan Li, Yuanlong |
author_sort | Xie, Dong-Mei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-10272649 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-102726492023-06-17 Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway Xie, Dong-Mei Sun, Chuanwei Tu, Qingqiang Li, Suyi Zhang, Yu Mei, Xifan Li, Yuanlong J Tissue Eng Original Article 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. SAGE Publications 2023-06-12 /pmc/articles/PMC10272649/ /pubmed/37333896 http://dx.doi.org/10.1177/20417314231180033 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Xie, Dong-Mei Sun, Chuanwei Tu, Qingqiang Li, Suyi Zhang, Yu Mei, Xifan Li, Yuanlong Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title | Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title_full | Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title_fullStr | Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title_full_unstemmed | Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title_short | Modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the AKT signaling pathway |
title_sort | modified black phosphorus quantum dots promotes spinal cord injury repair by targeting the akt signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272649/ https://www.ncbi.nlm.nih.gov/pubmed/37333896 http://dx.doi.org/10.1177/20417314231180033 |
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