Key result
Luteolin nanoparticle composite hydrogel reduces infarct collagen fraction by ~25 percentage points in MI rats.
Why the study?
Luteolin is a promising natural flavonoid for treating myocardial infarction, but its poor water solubility, low bioavailability, and chemical instability severely hinder its clinical translation.
Does a local pH-responsive GelMA-KerMA composite hydrogel patch delivering luteolin-loaded PLGA nanoparticles improve cardiac function and promote myocardial repair compared to untreated MI or blank hydrogel controls in a rat model of acute myocardial infarction?
Does a local pH-responsive GelMA-KerMA composite hydrogel patch delivering luteolin-loaded PLGA nanoparticles improve cardiac function and promote myocardial repair compared to untreated MI or blank hydrogel controls in a rat model of acute myocardial infarction?
This preclinical study demonstrates that a pH-responsive GelMA-KerMA hydrogel patch loaded with luteolin-PLGA nanoparticles enables targeted local drug release in the acidic infarct microenvironment to promote multi-pathway myocardial repair.
Answers are grounded in this paper and cite their sources.
Should not change MI practice; hypothesis-generating for pH-responsive luteolin hydrogels in preclinical cardiac repair.
Myocardial infarction (MI) triggers cardiomyocyte apoptosis, oxidative stress imbalance, ventricular fibrosis, and impaired angiogenesis. Luteolin, a natural flavonoid compound, possesses antioxidant, anti-apoptotic, and cardioprotective properties, making it a promising candidate for MI treatment. However, its poor water solubility, low bioavailability, and chemical instability severely hinder its clinical translation. To address these limitations, we developed a photo-crosslinked composite hydrogel delivery system using gelatin methacryloyl and keratin methacryloyl (GelMA-KerMA). Luteolin-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles were uniformly dispersed within a three-dimensional gel network to achieve pH-triggered local drug delivery. The covalent GelMA-KerMA network retained structural integrity under both pH conditions. In the weakly acidic infarct microenvironment, acid-catalyzed hydrolysis of PLGA ester bonds was the primary driver of accelerated luteolin release, whereas the network mainly acted as a sustained-retarding reservoir. The incorporation of KerMA endowed the patch with enhanced mechanical stability and cytocompatibility, enabling better mechanical matching with the infarcted myocardium. The composite hydrogel promotes myocardial repair and functional recovery through the coordinated regulation of the rapid Akt/Bad phosphorylation cascade. It also sustains MAPK/Rap1-dependent transcriptional reprogramming. It inhibits mitochondrial apoptosis, scavenges reactive oxygen species (ROS), suppresses fibroblast activation, and promotes neovascularization. This study presents a protein-based delivery platform that integrates tailored physicochemical and mechanical properties with multi-pathway myocardial repair capabilities, offering a biomaterial strategy for minimally invasive local drug delivery in ischemic MI.
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Jiang et al. (2026) studied Myocardial infarction (preclinical rat LAD coronary artery ligation model) (n=30). GelMA-KerMA composite hydrogel delivering luteolin-loaded PLGA nanoparticles (GK@NPs) vs. Untreated MI model group, sham-operated group, blank GK hydrogel (MI + GK), and GK containing blank PLGA NPs (MI + GK@PLGA) was evaluated on Infarct area collagen volume fraction (CVF) at day 28. Luteolin-loaded PLGA nanoparticle composite hydrogel reduced infarct collagen volume fraction from 37.2% to 11.9% at 28 days and cardiomyocyte apoptosis from 2.72% to 0.68% at day 3 in MI rats.
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