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Chondroitin sulfate functionalized nanozymes inhibit the inflammation feedback loop for enhanced atherosclerosis

Chenglong Wang1, Yufeng He2, Jun Tang3

  • 1Department of Pharmaceutical Sciences, School of Pharmacy, Southwest Medical University, Luzhou, Sichuan 646000, China.

International Journal of Biological Macromolecules
|October 29, 2024
PubMed

Insights

Engineered nanozymes target inflammation in atherosclerosis by restoring oxidative balance and blocking inflammatory feedback loops. This approach reduces macrophage activation and inhibits plaque progression, offering a novel therapeutic strategy.

Area of Science:

  • Biomaterials Science
  • Nanotechnology
  • Cardiovascular Research

Background:

  • Atherosclerosis (AS) involves metabolic dysregulation of reactive oxygen species (ROS) like superoxide anion (O2-) and hydrogen peroxide (H2O2) within atherosclerotic plaques.
  • This dysregulation activates inflammatory feedback loops involving IL-1β, TNF-α, and MCP-1, exacerbating inflammation between macrophages and vascular smooth muscle cells (VSMCs).

Purpose of the Study:

  • To develop a novel chondroitin sulfate (CS)-functionalized dual-targeted engineered nanozyme for atherosclerosis treatment.
  • To investigate the nanozyme's ability to target inflammatory cells and modulate oxidative stress and inflammatory pathways.

Main Methods:

  • Development of CS-Lip/PB@Rap, a nanozyme encapsulating mesoporous Prussian blue nanoparticles (PBs) loaded with rapamycin (Rap) within CS-modified liposomes.
  • CS functionalization for CD44 receptor targeting to inflammatory macrophages and VSMCs.
  • Evaluation of the nanozyme's enzyme-like activities, oxidative stress modulation, and effects on inflammatory signaling pathways (e.g., NF-κB).

Main Results:

  • CS-Lip/PB@Rap demonstrated targeted delivery to macrophages and VSMCs via CD44 receptors.
  • The nanozyme effectively modulated oxidative stress imbalance and inhibited the NF-κB pathway.
  • Inflammatory feedback loops (TNF-α, IL-1β, MCP-1) were blocked, reducing inflammatory macrophage production and VSMC phenotypic switching.
  • Reduced oxidative stress decreased oxidized low-density lipoprotein (ox-LDL), inhibiting foam cell formation and alleviating atherogenesis.

Conclusions:

  • Engineered nanozymes can effectively target atherosclerotic lesions and restore metabolic balance of ROS.
  • This nanozyme inhibits inflammatory crosstalk between macrophages and VSMCs by modulating the NF-κB pathway.
  • The developed nanozyme presents a promising strategy for alleviating atherosclerotic progression by reducing oxidative stress and inflammation.
Keywords:
Chondroitin sulfate functionalized nanozymesInflammation feedback loopIntercellular crosstalk

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