A biomimic anti-neuroinflammatory nanoplatform for active neutrophil extracellular traps targeting and spinal cord injury therapy

被引:2
|
作者
Tang, Chunming [2 ]
Jin, Yaoyao [4 ]
Wu, Min [2 ]
Jia, Feng [5 ]
Lu, Xiaowei [6 ]
Li, Jinyu [2 ]
Wu, Jie [2 ]
Zhu, Senlin [2 ]
Wang, Zhiji [2 ]
An, Di [1 ]
Xiong, Wu [3 ]
Zhang, Yongjie [3 ]
Xu, Huae [2 ]
Chen, Xufeng [1 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Emergency Med, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Sch Pharm, Dept Pharmaceut, Nanjing 211166, Peoples R China
[3] Nanjing Med Univ, Dept Human Anat, Nanjing 211166, Peoples R China
[4] Xuzhou Med Univ & Second Peoples Hosp Huaian, Affiliated Huaian Hosp, Dept Emergency, Huaian 223022, Peoples R China
[5] Nanjing Univ, Yancheng Peoples Hosp 1, Affiliated Yancheng Hosp 1, Dept Neurosurg,Med Sch, Yancheng 224008, Peoples R China
[6] Nanjing Med Univ, Affiliated Hosp 1, Dept Geriatr Neurol, Nanjing 210029, Peoples R China
关键词
Hybrid cell membrane; DNAse I conjugating; Neutrophil extracellular traps; Neutrophil hijacking; NF-kappa B; Spinal cord injury; METHYLPREDNISOLONE; INFLAMMATION; PROMOTE; DNA;
D O I
10.1016/j.mtbio.2024.101218
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Traumatic spinal cord injury (SCI) always leads to severe neurological deficits and permanent damage. Neuroinflammation is a vital process of SCI and have become a promising target for SCI treatment. However, the neuroinflammation-targeted therapy would hinder the functional recovery of spinal cord and lead to the treatment failure. Herein, a biomimic anti-neuroinflammatory nanoplatform (DHCNPs) was developed for active neutrophil extracellular traps (NETs) targeting and SCI treatment. The curcumin-loaded liposome with the antiinflammatory property acted as the core of the DHCNPs. Platelet membrane and neutrophil membrane were fused to form the biomimic hybrid membrane of the DHCNPs for hijacking neutrophils and neutralizing the elevated neutrophil-related proinflammatory cytokines, respectively. DNAse I modification on the hybrid membrane could achieve NETs degradation, blood spinal cord barrier, and neuron repair. Further studies proved that the DHCNPs could reprogram the multifaceted neuroinflammation and reverse the SCI process via nuclear factor kappa-B (NF-kappa B) pathway. We believe that the current study provides a new perspective for neuroinflammation inhibition and may shed new light on the treatment of SCI.
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页数:16
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