By modulating these critical molecular processes, it is possible to restore redox balance, protect cardiomyocytes from lethal oxidative stress, and ultimately attenuate the progression of myocardial injury and other ferroptosis-related cardiovascular pathologies
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In myocardial I/R, BPC 157 reduced oxidative stress markers and MDA levels while preserving cardiac tissue.50 In hippocampal I/R, it attenuated neuronal injury by modulating key regulatory genes early growth response 1 (Egr1), AKT serine/threonine kinase 1 (Akt1), Kirsten rat sarcoma viral oncogene homolog (Kras), proto-oncogene tyrosine-protein kinase Src (Src), vascular endothelial growth factor receptor 2 (VEGFR2), nitric oxide synthase 3 (NOS3), and nitric oxide synthase 1 (NOS1)and suppressing nitric oxide synthase 2 (NOS2) and NF-B signaling, highlighting its ability to influence multiple ROS-related pathways.63 Experimental study in Drosophila melanogaster also demonstrated that BPC 157 significantly improved survival under hydrogen peroxideinduced oxidative stress, suggesting that its protective effects extend to hydrogen peroxidedependent pathways of ROS toxicity.88 Our findings extend this evidence by directly demonstrating modulation of TAS and TOS in skeletal muscle I/R injury
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