The effect of dipicolinic acid on the oxidative status, activity of antioxidant enzymes and heat shock proteins in diclofenac-induced myocardial injury in rats.

The aim of the study was to evaluate the cardioprotective potential of dipicolinic acid (DPA) and its effect on oxidative status and the functioning of superoxide dismutase, catalase and heat shock proteins in a model of diclofenac-induced myocardial injury. Rats were randomly assigned to four groups: control group; animals with diclofenac-induced myocardial injury; rats with pathology received intragastric injections of DPA at a dosage of 10 mg/kg; rats with pathology received DPA at a dosage of 20 mg/kg. The results of the study showed that the administration of DPA to rats with myocardial damage induced by diclofenac led to a significant decrease in the activity of cardiomyocyte cytolytic marker enzymes. Additionally, the tested compound significantly decreased the parameters of bio-chemiluminescence, which reflect the intensity of free radical-induced oxidation. DPA restored the activity of aconitate hydratase, prevented citrate accumulation, and changed superoxide dismutase and catalase activity, and their genes mRNA levels toward control values. At the same time, the administration of DPA resulted in a normalization in total chaperone activity and the expression of mRNA of heat shock proteins. DPA injections also contributed to the normalization of mRNA levels for nuclear factor erythroid 2-associated factor 2 and hypoxia-inducible factor. The observed positive changes may be attributed to an improvement in myocardial metabolic processes as a result of DPA action, which may have antithrombotic effects and inhibit the activity of free radical-mediated oxidation of biological molecules.