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

Chunming Tang, Yaoyao Jin, Min Wu, Feng Jia, Xiaowei Lu et al.
Other Materials today. Bio 2024 18 اقتباسات
PubMed DOI
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Study Design

نوع الدراسة
Other
المجتمع المدروس
Traumatic spinal cord injury model
التدخل
A biomimic anti-neuroinflammatory nanoplatform for active neutrophil extracellular traps targeting and spinal cord injury therapy. None
المقارن
SCI model controls
النتيجة الأولية
NETs targeting and spinal cord injury recovery
اتجاه التأثير
Positive
خطر التحيز
Unclear

Abstract

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 anti-inflammatory 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-κB) pathway. We believe that the current study provides a new perspective for neuroinflammation inhibition and may shed new light on the treatment of SCI.

باختصار

A biomimic anti-neuroinflammatory nanoplatform developed for active neutrophil extracellular traps (NETs) targeting and SCI treatment and proved that the DHCNPs could reprogram the multifaceted neuroinflammation and reverse the SCI process via nuclear factor kappa-B (NF-κB) pathway.

Used In Evidence Reviews

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