Fraxetin attenuates ferroptosis in myocardial infarction via AKT/Nrf2/HO-1 signaling.
Yifei Xu, Haiyan Lin, Huan Wang, Jie Pang, Ying Zhou
Abstract
BACKGROUND: Myocardial infarction (MI) is the principal cause of mortality globally. Fraxetin (Fra) has anti-oxidative and anti-inflammatory properties. Nevertheless, the functional action of Fra in the progression of MI has never been elucidated. METHOD: , malondialdehyde (MDA), and glutathione (GSH). RESULTS: models. Notably, silencing Nrf2 enhanced the ferroptosis in H9C2 cells induced by OGD/R, while LY, an inhibitor of AKT phosphorylation, diminished the inhibition of Fra. CONCLUSION: Fra attenuated MI-induced ferroptosis via AKT/Nrf2/HO-1 signaling, providing a potential therapeutic agent for MI.
Topics & Concepts
Protein kinase BIn vivoPharmacologyMalondialdehydeViability assayApoptosisGlutathioneMyocardial infarctionGlutathione peroxidasePhosphorylationPI3K/AKT/mTOR pathwayChemistryMedicineGPX4Cancer researchOxidative stressInternal medicineBiochemistryBiologyEnzymeBiotechnologyFerroptosis and cancer prognosisCancer-related molecular mechanisms researchGDF15 and Related Biomarkers