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<p>Ulcerative colitis (UC) is a chronic, immune-mediated disorder with limited treatment efficacy due to drug resistance. As key immune effectors, Macrophages drive UC pathogenesis: The M1 polarization promoted through P-selectin/PSGL-1 binding between platelets and macrophages exacerbates inflammation. Rutin-PEG-PLGA nanoparticles (P@Rut) were engineered by encapsulating rutin in PEG-PLGA cores. Biomimetic platelet membrane nanoparticles (PP@Rut) were synthesized by extracting platelet membranes and coating P@Rut. The blockade of platelet-macrophage interactions by PP@Rut was assessed&#xa0;in vitro&#xa0;and&#xa0;in vivo. The inhibition of macrophage polarization and JNK/STAT1 pathway was evaluated via immunofluorescence (CD86/CD206) and RT-qPCR (IL-1β, TNF-α, TGF-β). Apoptosis was quantified using flow cytometry and TUNEL staining, complemented by Western blot analysis of apoptosis-related proteins(Bcl-xl, Bak, and cleaved-caspase3). Additionally, intestinal barrier integrity was assessed through tight junction protein expression (Occludin, Claudin-1, ZO-1), while therapeutic efficacy was determined via colon length, body weight, disease activity index (DAI) scores, and H&amp;E staining histopathological analysis. PP@Rut significantly shifted macrophage polarization from M1 to M2 through the JNK/STAT1 pathway, suppressed inflammatory response, reduced mucosal epithelial cells apoptosis, and improved intestinal barrier integrity. In DSS-induced mice, PP@Rut demonstrated higher accumulation in inflamed colon versus P@Rut, ameliorating body weight loss, DAI scores, colon shortening, and histopathological injury, including the reduction in inflammatory infiltration and crypt damage. PP@Rut represents a synergistic nanotherapeutic strategy that competitively inhibits platelet-macrophage binding to reprogram polarization, suppress inflammation, and restore barrier function in UC.</p>

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Bionic platelet membrane-coated rutin nanoparticles attenuate ulcerative colitis by suppressing platelet-mediated macrophage inflammation

  • 期刊论文

  • 发表日期：

    2025年12月26日

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  • Rong Zhang,
  • Ruya Mei,
  • Bingqing Liang,
  • Xinyue Zhang,
  • Tong Zhang,
  • Jie Luo,
  • Juhua Zhang,
  • Qin Pan,
  • Yuzhong Yan

摘要

Ulcerative colitis (UC) is a chronic, immune-mediated disorder with limited treatment efficacy due to drug resistance. As key immune effectors, Macrophages drive UC pathogenesis: The M1 polarization promoted through P-selectin/PSGL-1 binding between platelets and macrophages exacerbates inflammation. Rutin-PEG-PLGA nanoparticles (P@Rut) were engineered by encapsulating rutin in PEG-PLGA cores. Biomimetic platelet membrane nanoparticles (PP@Rut) were synthesized by extracting platelet membranes and coating P@Rut. The blockade of platelet-macrophage interactions by PP@Rut was assessed in vitro and in vivo. The inhibition of macrophage polarization and JNK/STAT1 pathway was evaluated via immunofluorescence (CD86/CD206) and RT-qPCR (IL-1β, TNF-α, TGF-β). Apoptosis was quantified using flow cytometry and TUNEL staining, complemented by Western blot analysis of apoptosis-related proteins(Bcl-xl, Bak, and cleaved-caspase3). Additionally, intestinal barrier integrity was assessed through tight junction protein expression (Occludin, Claudin-1, ZO-1), while therapeutic efficacy was determined via colon length, body weight, disease activity index (DAI) scores, and H&E staining histopathological analysis. PP@Rut significantly shifted macrophage polarization from M1 to M2 through the JNK/STAT1 pathway, suppressed inflammatory response, reduced mucosal epithelial cells apoptosis, and improved intestinal barrier integrity. In DSS-induced mice, PP@Rut demonstrated higher accumulation in inflamed colon versus P@Rut, ameliorating body weight loss, DAI scores, colon shortening, and histopathological injury, including the reduction in inflammatory infiltration and crypt damage. PP@Rut represents a synergistic nanotherapeutic strategy that competitively inhibits platelet-macrophage binding to reprogram polarization, suppress inflammation, and restore barrier function in UC.