A biomimetic MnO2 nanozyme–extracellular vesicle platform integrates ROS scavenging and epigenetic modulation to inhibit NLRP3 inflammasome activation in spinal cord injury

Oxidative stress–driven neuroinflammation is a major barrier to functional recovery after spinal cord injury (SCI). Although the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome plays a pivotal role in SCI pathology, effective strategies to simultaneously regulate upstream redox imbalance and inflammasome-associated epigenetic activation are lacking. We developed a biomimetic nanosystem consisting of manganese dioxide nanozymes coated with neural stem cell–derived extracellular vesicles (MnO 2 @EVs). MnO 2 @EVs were locally administered in a murine SCI model. Oxidative stress and mitochondrial function were assessed by dihydroethidium staining, adenosine triphosphate (ATP) quantification, and JC-1 assays. Inflammasome activation and epigenetic regulation were analyzed using Western blotting, enzyme-linked immunosorbent assays (ELISA), chromatin immunoprecipitation–qPCR, and siRNA-mediated knockdown. Proteomics, metabolomics, and single-cell RNA sequencing were employed to elucidate global molecular and cellular mechanisms. MnO 2 @EVs efficiently scavenged excess reactive oxygen species (ROS), restored mitochondrial bioenergetics, and significantly suppressed NLRP3 inflammasome activation. Mechanistically, MnO 2 @EVs inhibited EP300-mediated histone H3K27 acetylation enrichment at the Nlrp3 locus, leading to transcriptional repression of inflammasome signaling. Additionally, MnO 2 @EVs activated the Nrf2–glutathione antioxidant pathway and remodeled the immune microenvironment, markedly reducing inflammatory Nlrp3⁺ microglia populations. These molecular effects translated into improved locomotor function in SCI mice. This study demonstrates that a biomimetic nanozyme platform can integrate ROS clearance with epigenetic regulation to achieve precise immunomodulation after SCI, highlighting MnO 2 @EVs as a promising nanobiotechnology-based therapeutic strategy.

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Journal
Journal of Nanobiotechnology
Published
2026-09-30
DOI
https://doi.org/10.1186/s12951-026-04970-6
Primary Topic
Spinal Cord Injury Research
Type
article
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article

A biomimetic MnO2 nanozyme–extracellular vesicle platform integrates ROS scavenging and epigenetic modulation to inhibit NLRP3 inflammasome activation in spinal cord injury

Minjie Yang, Huihan Wang, Lijun Wang, Liangjie Lu
Journal of Nanobiotechnology
Spinal Cord Injury Research
article

A biomimetic MnO2 nanozyme–extracellular vesicle platform integrates ROS scavenging and epigenetic modulation to inhibit NLRP3 inflammasome activation in spinal cord injury

Minjie Yang, Huihan Wang, Lijun Wang, Liangjie Lu
article en

Abstract

Oxidative stress–driven neuroinflammation is a major barrier to functional recovery after spinal cord injury (SCI). Although the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome plays a pivotal role in SCI pathology, effective strategies to simultaneously regulate upstream redox imbalance and inflammasome-associated epigenetic activation are lacking. We developed a biomimetic nanosystem consisting of manganese dioxide nanozymes coated with neural stem cell–derived extracellular vesicles (MnO 2 @EVs). MnO 2 @EVs were locally administered in a murine SCI model. Oxidative stress and mitochondrial function were assessed by dihydroethidium staining, adenosine triphosphate (ATP) quantification, and JC-1 assays. Inflammasome activation and epigenetic regulation were analyzed using Western blotting, enzyme-linked immunosorbent assays (ELISA), chromatin immunoprecipitation–qPCR, and siRNA-mediated knockdown. Proteomics, metabolomics, and single-cell RNA sequencing were employed to elucidate global molecular and cellular mechanisms. MnO 2 @EVs efficiently scavenged excess reactive oxygen species (ROS), restored mitochondrial bioenergetics, and significantly suppressed NLRP3 inflammasome activation. Mechanistically, MnO 2 @EVs inhibited EP300-mediated histone H3K27 acetylation enrichment at the Nlrp3 locus, leading to transcriptional repression of inflammasome signaling. Additionally, MnO 2 @EVs activated the Nrf2–glutathione antioxidant pathway and remodeled the immune microenvironment, markedly reducing inflammatory Nlrp3⁺ microglia populations. These molecular effects translated into improved locomotor function in SCI mice. This study demonstrates that a biomimetic nanozyme platform can integrate ROS clearance with epigenetic regulation to achieve precise immunomodulation after SCI, highlighting MnO 2 @EVs as a promising nanobiotechnology-based therapeutic strategy.

Journal of Nanobiotechnology
Zhengzhou University (CN), Jiujiang First People's Hospital (CN), Ningbo Medical Center Lihuili Hospital (CN), First Hospital of Jilin University (CN), Zhengzhou Central Hospital (CN)
Openalex Percentile: Top 12%
Spinal Cord Injury Research
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