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Updated: Jun 3, 2025

Synthesis of Monocyte-targeting Peptide Amphiphile Micelles for Imaging of Atherosclerosis
Published on: November 17, 2017
Application of therapeutical nanoparticles with neutrophil membrane camouflaging for inflammatory plaques targeting
Ningnannan Zhang1, Tianzhu Zhang1, Jintang Feng1
1Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, 300052, PR China.
Insights
Neutrophil membrane-cloaked nanoparticles loaded with simvastatin effectively target atherosclerotic plaques. This biomimetic nanoplatform enhances drug delivery, reduces plaque inflammation, and shows no toxicity, offering a novel approach for atherosclerosis management.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Cardiovascular Research
Background:
- Atherosclerosis is a primary cause of cardiovascular disease and myocardial infarction.
- Targeting atherosclerotic plaques is crucial for effective treatment across disease stages.
- Neutrophils naturally infiltrate atherosclerotic plaques, suggesting their recruitment mechanisms can be mimicked for therapeutic delivery.
Purpose of the Study:
- To develop a simvastatin-loaded, neutrophil membrane-cloaked nanoplatform (NNPST) for enhanced atherosclerosis management.
- To investigate the plaque-targeting capabilities and therapeutic efficacy of NNPST in vivo.
- To assess the biosafety of the neutrophil membrane-camouflaged nanoparticles.
Main Methods:
- Fabrication of simvastatin-loaded nanoparticles coated with neutrophil membranes (NNPST).
- Evaluation of NNPST's ability to mimic neutrophil function and evade phagocytosis.
- Assessment of plaque targeting and accumulation in ApoE-/- mice using dual-modality imaging (fluorescence/MR).
- Quantification of therapeutic effects on plaque size and local inflammation.
Main Results:
- NNPST demonstrated prolonged circulation time by evading macrophage phagocytosis.
- NNPST exhibited superior plaque homing in atherosclerotic mice compared to uncoated nanoparticles (NPST).
- NNPST treatment significantly reduced plaque burden (to 4.75 ± 1.48% of aortic area) by suppressing inflammatory macrophages.
- Biosafety assessments confirmed no noticeable toxicity associated with NNPST.
Conclusions:
- Neutrophil membrane-camouflaged nanoplatforms (NNPST) offer a promising strategy for targeted drug delivery in atherosclerosis.
- This biomimetic approach enhances therapeutic payload accumulation at plaque sites.
- The NNPST system provides a versatile platform for treating inflammatory diseases involving neutrophils.
Abstract:
Atherosclerosis is the leading cause of cardiovascular disease and myocardial infarction. Precise and effective plaque targeting is a major objective for therapeutic outcomes throughout various stages of atherosclerosis. Inspired by the natural recruitment of neutrophils in atherosclerotic plaques, we fabricated a simvastatin (ST)-loaded and neutrophil membrane-cloaked nanoplatform (NNPST) for enhancing localized payload delivery and atherosclerosis management. The resulting NNPST mimicked neutrophil function and significantly decreased macrophage-mediated phagocytosis to prolong its own circulation time in the blood. Compared to pristine nanoparticles (NPST) without a membrane coating, NNPST achieved better plaque targeting in ApoE-/- mice, as indicated by neutrophils actively recruited in atherosclerotic lesions. The higher plaque homing with NNPST was monitored by dynamic fluorescence/magnetic resonance (MR) dual-modality imaging. The results further showed that NNPST efficiently prevented atherosclerosis development mainly by suppressing local inflammatory macrophages, and the percentage of plaques in the entire aortic area was reduced to 4.75 ± 1.48 % following NNPST treatment. A biosafety assessment indicated that the biomimetic NNPST induced no noticeable toxicity in the body. This approach of neutrophil membrane-camouflaged nanoparticles offers new opportunities to various therapeutic agents for on-demand delivery in neutrophil-involved inflammatory diseases.
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