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Related Experiment Videos

Turmeric-derived nanovesicles reprogram pathological NETosis to mitigate inflammatory bone loss.

Ming Wang1,2,3,4, Kamoran Tuerhong1, Ying Xie1

  • 1The Affiliated Stomatological Hospital of Chongqing Medical University, Chongqing, 401147, China.

Journal of Nanobiotechnology
|June 18, 2026
PubMed

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Summary
This summary is machine-generated.

Turmeric-derived nanovesicles (TNVs) effectively target and reduce neutrophil extracellular traps (NETs) and inflammation, offering a novel therapy for periodontitis and other inflammatory bone loss conditions.

Area of Science:

  • Biomaterials Science
  • Immunology
  • Nanotechnology

Background:

  • Inflammatory bone destruction, like in periodontitis, involves persistent inflammation and osteoclast activity, often amplified by neutrophil extracellular traps (NETs).
  • Current therapies targeting NETs have limitations in efficiency, bioavailability, and safety, necessitating advanced delivery systems.
  • Aberrant NET formation and dysregulated inflammatory microenvironments create a self-amplifying cycle of bone loss.

Purpose of the Study:

  • To develop a novel biomimetic nanodelivery system for targeting NET formation and associated inflammatory pathways.
  • To investigate the therapeutic potential of turmeric-derived nanovesicles (TNVs) in preclinical models of inflammatory bone loss.

Main Methods:

  • Single-cell transcriptomic analysis of existing datasets to identify NET formation as a therapeutic target in periodontitis.
Keywords:
ImmunomodulationInflammation-associated accumulationInflammatory bone destructionNeutrophil extracellular trapsPathological NETosisPlant-derived extracellular vesicles

Related Experiment Videos

  • Development of TNVs from turmeric, characterized by their plant-derived lipid bilayer and bioactive cargo.
  • In vitro and in vivo studies in a murine periodontitis model to evaluate TNV efficacy in suppressing NETosis, inflammation, and bone resorption.

    • Main Results:

    • TNVs demonstrated biocompatibility and efficient uptake by neutrophils, significantly suppressing NET formation by reducing ROS, CitH3, MPO, ELANE expression, and extracellular DNA release.
    • Transcriptomic analysis confirmed TNVs downregulate NET-associated pathways and enhance antioxidant/anti-inflammatory responses.
    • In vivo, TNVs accumulated at inflamed sites, inhibited NET formation and osteoclastogenesis, reduced inflammation, mitigated bone loss, and preserved bone microarchitecture.

    Conclusions:

    • TNVs represent a promising plant-derived biomimetic nanoplatform for targeted delivery to inflamed tissues.
    • TNVs exhibit potent immunomodulatory effects, offering a novel therapeutic strategy for inflammation-induced bone loss, including periodontitis.
    • The integrated bioactive cargo and efficient delivery capacity of TNVs provide a compelling approach to combatting inflammatory bone destruction.