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  11. Delphinidin Inhibits The Alox15-mediated Ferroptosis In Rats To Alleviate Myocardial Ischemia And Reperfusion Injury

Delphinidin inhibits the ALOX15-mediated ferroptosis in rats to alleviate myocardial ischemia and reperfusion injury

Qing Sun1, Mei Lv2, Zhen Wang1

  • 1Department of Cardiology, Yantaishan Hospital, No.10087, Science and Technology Avenue, Laishan District, Yantai 264000, Shandong, China.

Biochimica Et Biophysica Acta. Molecular Cell Research
|June 13, 2025

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View abstract on PubMed

Summary
This summary is machine-generated.

Delphinidin (Dp) protects against myocardial ischemia-reperfusion injury (MIRI) by inhibiting ferroptosis. It achieves this by binding to ALOX15, promoting its degradation and improving cardiac function.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Myocardial ischemia-reperfusion injury (MIRI) is a critical clinical condition.
  • Understanding the molecular mechanisms of MIRI is essential for developing effective treatments.
  • Ferroptosis, a form of regulated cell death, plays a significant role in MIRI pathogenesis.

Purpose of the Study:

  • To investigate the protective role of delphinidin (Dp) in MIRI.
  • To elucidate the underlying molecular mechanisms of Dp's action in MIRI.
  • To determine if Dp affects ferroptosis in the context of MIRI.

Main Methods:

  • Established MIRI rat models and primary cardiomyocyte/H9C2 cell models.
  • Assessed cardiac function and myocardial infarction using ultrasound and histological staining.
Keywords:
ALOX15DelphinidinFerroptosisMIRI

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  • Utilized cell counting kit-8 assay, flow cytometry, Western blotting, and qPCR to analyze cell viability, apoptosis, and ALOX15 expression.
  • Detected ferroptosis-related factors and lactate dehydrogenase levels.

    • Main Results:

    • Delphinidin (Dp) dose-dependently improved cardiac function (EF, FS) and reduced cardiac damage in MIRI rats.
    • Dp treatment inhibited cardiomyocyte apoptosis and ferroptosis both in vivo and in vitro.
    • Molecular docking revealed Dp binds to ALOX15, inducing its degradation and thereby reducing ferroptosis.
    • Overexpression of ALOX15 or treatment with erastin reversed Dp's protective effects.

    Conclusions:

    • Delphinidin (Dp) exerts protective effects against myocardial ischemia-reperfusion injury (MIRI).
    • Dp inhibits ferroptosis by targeting and degrading the ferroptosis-related protein ALOX15.
    • These findings highlight Dp as a potential therapeutic agent for MIRI.