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<p>Vulnerable atherosclerotic plaque rupture is closely associated with macrophage-driven inflammation induced by oxidized low-density lipoprotein (ox-LDL). Although isoliquiritigenin (ISL) possesses potent anti-inflammatory activity, its therapeutic application is limited by poor aqueous solubility and low cellular uptake. In this study, an amphiphilic peptide (APD) was designed to construct a nanoscale delivery system for ISL. The resulting APD@ISL nanoparticles exhibited uniform particle size, good colloidal stability, and pH-responsive drug release behavior. Cellular experiments showed that APD@ISL significantly enhanced the intracellular delivery of ISL and effectively alleviated ox-LDL-induced macrophage lipotoxicity. Mechanistically, APD@ISL suppressed the expression of pro-inflammatory markers (TNF-α, IL-6, and iNOS) while promoting anti-inflammatory markers (IL-10 and Arg-1), indicating a macrophage polarization shift from the M1 to the M2 phenotype. Overall, the APD-based nanocarrier improves the bioavailability and anti-inflammatory efficacy of ISL, providing a promising nanomedicine strategy for stabilizing vulnerable atherosclerotic plaques.</p>

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Amphiphilic peptide-based nanoscale delivery of isoliquiritigenin attenuates ox-LDL-induced macrophage inflammation

  • 期刊论文

  • 发表日期：

    2026年7月13日

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  • Yanwei Ye,
  • Yiting Yang,
  • Yingying Wen,
  • Xiaochao Zhang,
  • Dongxia Yan

摘要

Vulnerable atherosclerotic plaque rupture is closely associated with macrophage-driven inflammation induced by oxidized low-density lipoprotein (ox-LDL). Although isoliquiritigenin (ISL) possesses potent anti-inflammatory activity, its therapeutic application is limited by poor aqueous solubility and low cellular uptake. In this study, an amphiphilic peptide (APD) was designed to construct a nanoscale delivery system for ISL. The resulting APD@ISL nanoparticles exhibited uniform particle size, good colloidal stability, and pH-responsive drug release behavior. Cellular experiments showed that APD@ISL significantly enhanced the intracellular delivery of ISL and effectively alleviated ox-LDL-induced macrophage lipotoxicity. Mechanistically, APD@ISL suppressed the expression of pro-inflammatory markers (TNF-α, IL-6, and iNOS) while promoting anti-inflammatory markers (IL-10 and Arg-1), indicating a macrophage polarization shift from the M1 to the M2 phenotype. Overall, the APD-based nanocarrier improves the bioavailability and anti-inflammatory efficacy of ISL, providing a promising nanomedicine strategy for stabilizing vulnerable atherosclerotic plaques.