Abstract

Vascular disease remains the leading cause of death and disability, the etiology of which often involves atherosclerosis. The current treatment of atherosclerosis by pharmacotherapy has limited therapeutic efficacy. Here we report a biomimetic drug delivery system derived from macrophage membrane coated ROS-responsive nanoparticles (NPs). The macrophage membrane not only avoids the clearance of NPs from the reticuloendothelial system, but also leads NPs to the inflammatory tissues, where the ROS-responsiveness of NPs enables specific payload release. Moreover, the macrophage membrane sequesters proinflammatory cytokines to suppress local inflammation. The synergistic effects of pharmacotherapy and inflammatory cytokines sequestration from such a biomimetic drug delivery system lead to improved therapeutic efficacy in atherosclerosis. Comparison to macrophage internalized with ROS-responsive NPs, as a live-cell based drug delivery system for treatment of atherosclerosis, suggests that cell membrane coated drug delivery approach is likely more suitable for dealing with an inflammatory disease than the live-cell approach.

Highlights

  • Vascular disease remains the leading cause of death and disability, the etiology of which often involves atherosclerosis

  • NPs loaded with hydrophobic AT (AT-NPs), with a drug encapsulation efficiency (DEE) of 48.3% and a drug loading content (DLC) of 5.1%, were obtained by a simple selfassembly process (Fig. 1a)

  • It is well known that H2O2 oxidizes arylboronic esters[29,30], OxiCOS would degrade into pinacol borate, COS, and p-hydroxymethylphenol in the presence of H2O2

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Summary

Introduction

Vascular disease remains the leading cause of death and disability, the etiology of which often involves atherosclerosis. These data demonstrated the ROS responsiveness of AT-NPs and MM-AT-NPs in vitro, as well as their attenuation effects on LPS induced inflammation and oxLDL induced foam cell formation from macrophage, suggesting a significant potential of these biomaterials for atherosclerosis therapy.

Results
Conclusion

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