Cinnamic acid ameliorates myocardial injury caused by arsenic trioxide in rats by modulating oxidative stress and...

Cinnamic acid (CA), the primary bioactive component of cinnamon bark, exhibits therapeutic potential against myocardial injury. This study examined CA's cardioprotective effects in a rat myocardial injury model induced by arsenic trioxide (ATO). CA treatment significantly reduced cardiac enzyme levels and pathological changes versus ATO controls. It decreased Reactive Oxygen Species production, upregulated Nuclear factor erythroid 2-related factor 2/Glutathione S-Transferase Mu 2 transcription, enhanced antioxidant activities, and reduced inflammatory markers. Transmission Electron Microscopy demonstrated preserved mitochondrial ultrastructure. Western blot analysis revealed that CA elevated B-cell lymphoma-2 while suppressing pro-apoptotic proteins, and enhanced AMP-activated protein kinase α2 (AMPKα2), phosphorylated AMPKα2 (p-AMPKα2), Sirtuin 1 (SIRT1) and Proliferator-activated receptor-gamma coactivator 1α (PGC-1α) expression. Molecular docking confirmed the robust binding affinity of CA toward pathway-associated proteins. These findings indicate CA alleviates ATO-induced myocardial injury through AMPKα2/SIRT1/PGC-1α pathway modulation, suppressing Reactive Oxygen Species, oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis.