Effects of zofenopril and nebivolol on TRPM2 channels expression in myocardial infarction

ABSTRACT EFFECTS OF ZOFENOPRIL AND NEBIVOLOL ON TRPM2 CHANNELS EXPRESSION IN MYOCARDIAL INFARCTION The pathophysiology of Myocardial Infarction (MI) is not clear yet. In this study, we aimed to investigate the effects of Zofenopril and Nebivolol on Transient Receptor Potential Melastatin 2 (TRPM2) cation channels in the heart tissues of rats with Isoproterenol (ISO) induced myocardial infarction. In the study, 48 Sprague Dowley strain male rats weighing between 210 to 280 g were used. Totally 8 groups were performed as 6 animals in each group. During the 21 days test period, no application was applied to control group. 150 mg/kg of isoproterenol, 2 times for 24 hours interval were given subcutaneously to MI group. After MI induction, treatment groups received Zofenopril (MI+Z), Nebivolol (MI+N), Zofenopril+Nebivolol (MI+Z+N) orally during the experiment period. In Sham groups MI induction was not performed and they received Zofenopril (Z), Nebivolol (N), Zofenopril+Nebivolol (Z+N) orally. At the end of the experiment the rats decapitated under anaesthesia and from removed heart tisues TRPM2 levels were measured by Polymerase Chain Reaction (PCR) and immunohistochemical methods. TRPM2 levels were not statistically significantly different between control and Sham ( Nebivolol, Zofenopril and Zofenopril + Nebivolol) groups. TRPM2 levels of MI group were found to be significantly lower in comparison with control group (p<0.05). TRPM2 levels of MI group were significantly lower than Sham groups (p<0.05). TRPM2 levels were not statistically significantly different between MI and MI+Nebivolol, MI+Zofenopril, MI+Zofenopril + Nebivolol groups. In conclusion; TRPM2 channels may contribute to pathophysiological mechanisms of MI. With future studies we will be able to understand the role of TRPM2 cation channels on MI pathophysiology. Keywords: Myocardial Infarction, TRPM2, Zofenopril, Nebivolol.