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During ischemia, mitochondrial dysfunction leads to adenosine triphosphate (ATP) depletion, ionic imbalance, and metabolic acidosis, which compromise cellular integrity.11,13,14 Upon reperfusion, a rapid surge in reactive oxygen species (ROS) occurs via multiple enzymatic sources, including xanthine oxidase, NADPH oxidase, the mitochondrial electron transport chain, and uncoupled nitric oxide synthase.1518 These ROSsuch as superoxide anion (O), hydrogen peroxide (HO), hydroxyl radical (OH), and peroxynitrite (ONOO)induce lipid peroxidation, protein oxidation, and DNA damage, thereby activating cell death pathways including apoptosis, necrosis, necroptosis, and autophagy.13,1921 In parallel, reperfusion initiates robust inflammatory responses characterized by interleukin-6 (IL-6) upregulation, neutrophil infiltration, and cytokine release, alongside endothelial dysfunction, leukocyte adhesion, and complement activation.18,20,22 These processes involve key molecular mediatorsincluding hypoxia-inducible factor 1-alpha (HIF-1), vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), p53, B-cell lymphoma 2 (Bcl-2), Bcl-2associated X protein (Bax), and cysteine- aspartate protease-3 (Caspase-3)which regulate oxidative stress responses, angiogenesis, and apoptosis, with their imbalance determining tissue survival or loss.2325 Furthermore, the interplay between oxidative stress, inflammation, and apoptosis is closely linked to activation of signaling pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B), a central regulator in the pathogenesis of tissue injury