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

被引:12
|
作者
Xie, Dong-Mei [3 ]
Sun, Chuanwei [1 ]
Tu, Qingqiang [4 ]
Li, Suyi [1 ,2 ]
Zhang, Yu [1 ,2 ]
Mei, Xifan [5 ]
Li, Yuanlong [1 ,2 ]
机构
[1] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Cardiovasc Inst, Guangdong Acad Med Sci, Guangzhou, Peoples R China
[2] Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Dept Orthoped, Zhongshan Rd 2, Guangzhou 510080, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Cardiol, Guangzhou, Peoples R China
[4] Sun Yat Sen Univ, Zhongshan Med Coll, Guangzhou, Peoples R China
[5] Jinzhou Med Univ, Affiliated Hosp 3, Dept Orthoped, Jinzhou 121001, Peoples R China
基金
中国博士后科学基金;
关键词
Spinal cord injury; black phosphorus quantum dots; anti-inflammation; neuro-regeneration; AKT signaling pathway; CHONDROITIN SULFATE PROTEOGLYCANS; CELL-CYCLE; OLIGODENDROCYTE; REGENERATION; APOPTOSIS; PROTEINS; BIOLOGY; SYSTEM; MYELIN; MAPK;
D O I
10.1177/20417314231180033
中图分类号
Q813 [细胞工程];
学科分类号
摘要
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.
引用
收藏
页数:19
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