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April 24, 2026SHILAP Revista de lepidopterología0 citationsOpen Access

Methyl eugenol attenuates age-associated oxidative fragility by coupling Ca2+-calpain inhibition with Band 3 stabilization in human erythrocytes

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JZJiasi ZhangQLQi LiYDYilan Dai

Key Points

  • The study aims to explore whether methyl eugenol (ME) stabilizes Band 3 in erythrocytes against oxidative damage due to aging.
  • Erythrocytes were treated with hydrogen peroxide to simulate oxidative stress.
  • Hemolysis assays, SEM, flow cytometry, and Western blotting assessed damage and Band 3 function.
  • In silico docking studies analyzed interactions between ME metabolites and Band 3.
  • ME effectively preserved erythrocyte morphology at an optimal concentration of 2 µM.
  • Treatment significantly reduced intracellular oxidative stress, enhancing cell viability.
  • ME stabilized the full-length and cytoplasmic domains of Band 3 while inhibiting calpain activity.

Abstract

Background Human erythrocytes serve as an ideal model for cellular aging, a process where longevity relies on membrane scaffold integrity. The oxidative deterioration of Band 3, a major integral membrane protein, is a central driver of this senescence. This study investigated whether methyl eugenol (ME) stabilizes Band 3 against age-associated oxidative fragility. Methods Erythrocytes were challenged with H 2 O 2 to simulate age-associated oxidative injury. Damage was evaluated via hemolysis assays, SEM, and flow cytometry. Sulfate (SO 4 2- ) uptake kinetics and Western blotting were employed to assess Band 3 anion exchange function and structural stability. In silico docking simulated interactions between ME metabolites and the Band 3 structure. Physiological relevance was validated in a human cohort (n = 81; 20–90 years) via regression and stratified analyses of glutathione (GSH) and malondialdehyde (MDA) levels. Results ME exhibited an optimal protective concentration at 2 µM, effectively preserving biconcave morphology and attenuating hemolysis. Treatment significantly mitigated intracellular oxidative stress and rescued cell viability. Mechanistically, ME suppressed the pathological increase in intracellular Ca 2+ concentration and inhibited calpain activity. Functionally, ME significantly restored sulfate transport rates. Western blotting confirmed that ME specifically preserved the full-length (100 kDa) and cytoplasmic (43 kDa) domains of Band 3, whereas the 55 kDa transmembrane domain remained largely unaffected. Docking simulations predicted a specific interaction with residue ARG292 within the cytoplasmic domain, suggesting a structural basis for this stabilization. In the donor cohort, ME extended the projected GSH half-life (from 47.14 to 64.14 years) and reduced maximal lipid peroxidation by ~40%. Conclusion ME mitigates oxidative eryptosis by coupling Ca 2+ –calpain inhibition with site-specific Band 3 stabilization, offering a rationale for using ME to standardize erythrocyte quality and reduce age-associated fragility.

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Cite This Study

Zhang et al. (2026) studied this question.

synapsesocial.com/papers/69eb07a4553a5433e34b3314https://doi.org/10.3389/fphys.2026.1796160
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