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April 5, 2026World Journal of Traditional Chinese MedicineOpen Access

Baicalein Ameliorates ALOX15-mediated Lipid Peroxidation in Mitochondria and Protects Cardiomyocytes against Palmitate Acid-induced Ferroptosis through the ACSL4/ALOX15/GPX4 Axis

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Authors

LDLin-Yue DongLFLi-Ye FangDHDoudou Huang

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Overview

Investigating baicalein's effects on ferroptosis in cardiomyocytes, indicating its potential in combating diabetic cardiomyopathy.

Key Points

  • This research aims to explore how baicalein impacts ferroptosis in cardiomyocytes exposed to elevated free fatty acid levels.
  • H9c2 cardiomyocytes were treated with palmitate to induce ferroptosis.
  • Lipid peroxidation and reactive oxygen species (ROS) levels were measured.
  • Mitochondrial function indicators such as membrane potential and cytochrome c release were assessed.
  • Protein expression levels of GPX4, ACSL4, and ALOX15 were analyzed by Western blot.
  • Statistical analysis determined the concentration-dependent effects of treatments.
  • Palmitate increased lipid peroxidation and ROS levels in a concentration-dependent manner.
  • Baicalein inhibited ALOX15-mediated 12-, 15-HETE production and lipid peroxidation.
  • Baicalein improved mitochondrial dysfunction by restoring membrane potential and reducing cytochrome c release.
  • Treatment with baicalein increased GPX4 levels while decreasing ACSL4 and ALOX15 expression in H9c2 cells.

Cite This Study

Dong et al. (2026) studied this question.

synapsesocial.com/papers/69d1fca7a79560c99a0a2455https://doi.org/10.4103/wjtcm.wjtcm_76_25
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