ArticleJournal of nanobiotechnology2025
Apigenin regulates CCR5/JAK1/STAT1/MMPs signaling to alleviate secondary brain injury after intracerebral hemorrhage and its enhanced delivery via targeted nanoparticles.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- pH-responsive CDs-based nanoplatform for chemo-resistant esophageal cancer treatment via downregulation of HIF-1α related pathway.Journal of nanobiotechnology · 2026Article
- Where and when to strike: Spatiotemporally controlled smart nanomedicines for precision antibacterial therapy.Acta pharmaceutica Sinica. B · 2026Review
- Advancing Parkinson's Prevention: Brain-Specific Lipopolyplex Delivery of the GDNF as a Neuroprotective Gene Therapy.ACS materials Au · 2026Article
- The antifibrotic effects of a click chemistry-based albumin nanocomplex in an idiopathic pulmonary fibrosis model.Journal of nanobiotechnology · 2026Article
- Ependymal cell inflammatory activation in response to intracerebral hemorrhage.Journal of neuroinflammation · 2026Article
- Apigenin accelerates fracture healing by enhancing endochondral differentiation and inflammation resolution via targeting NF-κB signaling.Frontiers in immunology · 2026Article
- Macrophage Membrane-Camouflaged Mesoporous Polydopamine Nanoparticles for Targeted Delivery of Apigenin in Sepsis-Induced Acute Lung Injury.International journal of nanomedicine · 2026Article
- Computational pharmacovigilance of tranexamic acid: implications for intracerebral hemorrhage based on FAERS database and network toxicology.Frontiers in pharmacology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Intracerebral hemorrhage (ICH), a severe cerebrovascular disorder with high mortality, leads to secondary brain injury (SBI) primarily through neuroinflammation and blood-brain barrier (BBB) disruption. Among the pathological cascades, excessive activation of macrophages and the CCR5/JAK1/STAT1/MMPs signaling pathway play pivotal roles in amplifying neuronal damage. Apigenin (API), a natural flavonoid with anti-inflammatory and neuroprotective properties, has emerged as a promising therapeutic candidate to counteract these processes. In this study, we developed apigenin-loaded PLGA nanoparticles functionalized with DSPE-PEG2000-RVG29 and DSPE-PEG2000-folic acid (RVG/FA-NPs@API) to achieve targeted delivery to inflammatory macrophages and investigated their therapeutic effects against SBI after ICH. In a murine ICH model, API administration significantly improved neurological outcomes, reduced cerebral edema, suppressed neuronal apoptosis, and preserved BBB integrity. Mechanistically, API bound covalently to JAK1 at Cys1052, inhibiting its phosphorylation and subsequently downregulating the CCR5/JAK1/STAT1/MMPs cascade. Furthermore, RVG/FA-NPs@API demonstrated excellent stability, efficient brain-targeting, and superior biocompatibility, achieving enhanced therapeutic efficacy compared with free API. These findings highlight a novel strategy for targeted immunomodulation and provide translational insights into nanoparticle-assisted delivery of natural compounds for the treatment of ICH-induced SBI.
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