Effects of cilostazol on the intensity of lipid peroxide oxidation (LPO) process in rats with a model of myocardial ischemia-reperfusion (IR) injury

Aim: One of the primary factors in the pathogenesis of morphofunctional processes occurring in the myocardium under anoxic ischemia and reperfusion injury is the formation of highly toxic reactive oxygen species (ROS) and subsequent peroxide oxidation. This oxidative damage results in the breakdown of structural lipids, leading to disrupted transmembrane ion permeability, reduced contractility, dangerous arrhythmias, and hemodynamic disorders. To investigate the changes in levels of the Superoxide Dismutase (SOD) and Glutathione Peroxidase (GSH-Px) enzymes and malondialdehyde (MDA) in a myocardial ischemia-reperfusion (IR) injury model in rats, as well as the effects of prophylactic cilostazol on these parameters. Material and Methods: The study was conducted on 24 Wistar Albino rats divided into three groups of eight animals each. In the control group, no coronary occlusion was performed, while in the IR group, acute ischemia was induced via Left Anterior Descending artery (LAD) compression for 45 minutes, followed by 180 minutes of reperfusion. In the cilostazol group, 20 mg/kg/day of cilostazol was administered via gavage for two weeks before IR induction. Levels of SOD and GSH-Px enzymes and MDA in the blood were evaluated to assess lipid peroxidation (LPO) activity. Results: The SOD level was 67.28±4.77 ng/l in the control group, rising to 118.26±5.75 ng/l in the IR group and 100.64±6.90 ng/l in the cilostazol group (P=0.009); the difference between groups was not statistically significant (P>0.05). While the GSH-Px level remained unchanged in the IR group, it more than doubled in the cilostazol group (P=0.02). The amount of MDA increased sixfold in the IR group compared to the control (P<0.001) but only doubled in the cilostazol group, making it 2.5 times lower than in the IR group (P<0.001). Conclusion: Administering cilostazol before establishing the IR model prevents critical activation of LPO. This antioxidant effect is attributed to increased activity of both SOD and GSH-Px enzymes.