Objective: It has been thought that Transient receptor potential melastatin 2 (TRPM2) cation channels can be activated by oxidative stress and these channels may be potential therapeutic targets in myocardial infarction. The main purpose of this study is to investigate the expression of TRPM2 cation channels in a rat myocardial ischemia-reperfusion model and the effects of Zofenopril and Nebivolol on the expression of these channels.

Materials and Methods: In the study, 8 groups were created, with 6 animals in each group. To the myocardial infarction (ME) group, 150 mg/kg Isoproterenol was given subcutaneously twice with an interval of 24 hours. Following the occurrence of ME, Zofenopril (ME+Z), Nebivolol (ME+N), Zofenopril + Nebivolol (ME+Z+N) were administered orally to the treatment groups throughout the experiment. To the sham groups, only Zofenopril, Nebivolol and Zofenopril + Nebivolol were given orally throughout the experiment without causing ME. At the end of the experiment, TRPM2 levels were measured using polymerase chain reaction and immunohistochemical methods.

Results: As a result of the studies; no statistically significant difference was observed in TRPM2 levels when the control group was compared with the Sham groups. Compared to the control group, TRPM2 level was found to be statistically significantly lower in the ME group. Compared to the sham groups, TRPM2 level was found to be statistically significantly lower in the ME group. Compared with the ME group, no statistically significant difference was observed in TRPM2 levels in the ME + Nebivolol, ME + Zofenopril and ME + Zofenopril + Nebivolol groups.

Conclusion: TRPM2 channels may contribute to the pathophysiological mechanism of ME.