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Peptide Extract from Apricot Kernels Mitigates Damage in Human Aortic Endothelial Cells Induced by Polystyrene Microplastics through theInhibition of the NLRP3 Signaling Pathway
Summary
Researchers found that a peptide extract from apricot kernels protects human aortic endothelial cells from polystyrene microplastic-induced damage by simultaneously suppressing NLRP3 inflammasome activation and reducing oxidative stress through Wnt/β-catenin pathway inhibition, reducing apoptosis by 39.1% and inflammatory cytokines by 17–38%.
Introduction: Polystyrene microplastics (PS-MPs) contribute to cardiovascular pathologies by inducing vascular endothelial injury through oxidative stress and inflammation. This study aimed to investigate the protective role of apricot kernel peptide extract (AKPE) against PS-MPs- induced damage in human aortic endothelial cells (HAECs) and to elucidate the underlying molecular mechanisms. Methods: AKPE was isolated from apricot kernels using an activity-guided fractionation approach based on its protective efficacy in HAECs exposed to PS-MPs. Cytotoxicity and dose-response experiments established an optimal concentration of 20 μM. Subsequent analyses included cell viability (CCK-8 assay), intracellular reactive oxygen species (ROS) and superoxide dismutase (SOD) activity, inflammatory cytokine levels (α, IL-1β, IL-18) via ELISA, apoptosis assessment by flow cytometry, and evaluation of mitochondrial function. Bioactive oligopeptides within AKPE were identified by mass spectrometry. The involvement of the NLRP3 inflammasome and Wnt/β-catenin signaling pathways was examined using Western blotting and quantitative PCR. Results: AKPE significantly counteracted the PS-MPs-induced reduction in HAEC viability, increasing it by 16.2% (p < 0.01). It also reduced intracellular ROS levels by 35.1% (p < 0.01) while preserving SOD activity. Furthermore, AKPE suppressed the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-18) by 17–38% (p < 0.01). PS-MPs-induced mitochondrial dysfunction and apoptosis were markedly attenuated, with a 39.1% decrease in apoptotic cells (p < 0.01). Mass spectrometry identified eight key oligopeptides as the primary bioactive constituents of AKPE. Mechanistically, these components acted synergistically to inhibit NLRP3 inflammasome activation and to modulate the dysregulated Wnt/β-catenin pathway. Discussion: AKPE protects HAECs from PS-MPs-induced damage through dual mechanisms: (1) suppressing NLRP3 inflammasome-driven inflammation and (2) mitigating oxidative stress via Wnt/β-catenin pathway inhibition. The synergy among AKPE peptides enhances resilience against PS-MPs, highlighting their potential as natural antioxidants. This study is the first to link apricot kernel peptides to PS-MPs-induced endothelial protection, providing novel insights into combating microplastic-related cardiovascular risks. Conclusion: AKPE exerts potent protective effects against oxidative and inflammatory injury in HAECs caused by PS-MPs. These effects are mediated by its constituent bioactive oligopeptides, which concurrently regulate the NLRP3 inflammasome and Wnt/β-catenin signaling pathways. Our findings highlight AKPE's potential as a promising natural therapeutic agent for alleviating vascular endothelial damage associated with microplastic exposure.
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