Dipicolinic Acid Exerts a Cardioprotective Effect Through Its Regulation of the Functioning of the Glutathione-Dependent Antioxidant System and Apoptosis in Diclofenac-Induced Myocardial Injury.

In this study, we evaluated the cardioprotective potential of dipicolinic acid (DPA) as well as its effect on the function of the glutathione-dependent antioxidant system and the intensity of apoptosis in diclofenac-induced injury. The study involved male white laboratory rats that were divided into four groups: a control group, animals that received diclofenac intraperitoneally at a dose of 10 mg/kg, on the background of Freund's complete adjuvant administration into the paw pad, and rats that received DPA at doses of 10 and 20 mg/kg in the context of pathology development. Findings of the study showed that administration of DPA to rats with myocardial damage induced by diclofenac led to a reduction in activity of markers for cardiac damage and an improvement in morphology of heart tissue. In addition, the tested compound was demonstrated to contribute to normalization in the concentrations of diene conjugates, α-tocopherol, and glutathione, as well as the functioning of antioxidant enzymes such as glutathione peroxidase, glutathione reductase, and glutathione transferase. Furthermore, it was observed that DPA affected the activity of glucose-6-phosphate dehydrogenase and NADP-dependent isocitrate dehydrogenase, which serve as suppliers of NADPH. Moreover, the administration of DPA resulted in a decrease in the activity of inductor caspase-8, caspase-9, and effector caspase-3, but not the level of apoptosis-inducing factor. The observed improvements may be attributed to enhanced myocardial metabolism under the influence of DPA, which has an antithrombotic effect and inhibits free radical-mediated oxidation of biological molecules.