ArticleJournal of nanobiotechnology2026
Targeting the oxidative microenvironment with a tannic acid-modified manganese dioxide nanozyme loaded with Honokiol nanoplatform to activate sirtuin 3-mediated deacetylation for alleviating cerebral ischemia-reperfusion injury.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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8 authors.
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Abstract
Cerebral ischemia-reperfusion injury (CIRI) is a major contributor to neurological dysfunction following stroke, with oxidative stress (OS) and mitochondrial dysfunction identified as key pathological mechanisms. To enable precise and efficient therapeutic intervention, we developed a redox-responsive smart nanoplatform, tannic acid-modified manganese dioxide nanozyme loaded with honokiol (MnO₂@TA@HNK), for the targeted delivery of Honokiol (HNK), a known Sirtuin 3 (SIRT3) activator, to enhance antioxidant defense pathways. Near-infrared fluorescence imaging and tissue distribution analyses confirmed the platform's selective accumulation in ischemic brain regions. Behavioral assessments and 2,3,5-Triphenyltetrazolium chloride (TTC) staining demonstrated that this nanoplatform significantly reduced infarct volume and improved neurological outcomes. Integrated multi-omics analysis revealed that the therapeutic effects are mediated through activation of the SIRT3/nuclear factor erythroid 2-related factor 2 (Nrf2)/Superoxide Dismutase 2 (SOD2) axis, promoting redox homeostasis. Furthermore, molecular docking and Co-Immunoprecipitation (Co-IP) experiments validated that this mechanism is dependent on SIRT3-mediated deacetylation. This study provides the first comprehensive elucidation of the synergistic regulation of mitochondrial antioxidant defenses via a nanozyme-co-delivered small molecule, offering a novel nanotherapeutic strategy for the treatment of CIRI.
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