ArticleDrug delivery and translational research2026
Bionic platelet membrane-coated rutin nanoparticles attenuate ulcerative colitis by suppressing platelet-mediated macrophage inflammation.
Article in Drug delivery and translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.