Effect of Nesfatin-1 on Ischaemia-Reperfusion Injury in Isolated Heart of Albino Rats

Abstract

Background: Nesfatin-1 is a hypothalamic neuropeptide which is involved in control of food intake and glucose homeostasis. Lower plasma level of Nesfatin-1 in patients with acute myocardial infarction (AMI) was reported. Objective: This study was designed to explore possible effect of Nesfatin-1 on ischemia-reperfusion injury in isolated heart of adult male albino rats and to explain the possible involved mechanisms, in a trial to clarify Nesfatin-1 expected cardioprotective effect. Design: This study was carried out on eighteen adult male albino rats which were divided equally (n=6) into 3 groups: Group I (ischemia-reperfusion I/R group); hearts were stabilized then subjected to (I/R) protocol, Group II (Nesfatin-1 preconditioning group); Nesfatin-1 was infused for 20 minutes before hearts were subjected to ischemia and Group III (Nesfatin-1 post-conditioning group); Nesfatin-1 was infused for 20 minutes at the beginning of 120 minutes of reperfusion. Cardiac performance indicators as left ventricular pressure (LVP), +max (LV dp/dt), -max (LVdP/dt)+, in addition to heart rate were recorded. Lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), superoxide dismutase (SOD) and C-reactive protein (CRP) were measured in the collected perfusate and cardiac Malondialdehyde (MDA) was measured. Finally, Nitro blue tetrazolium stain was used to detect the necrotic tissue percentage to the whole left ventricular mass. Results: In group III (post conditioning group), there was a significant increase of the studied cardiac parameters compared to group I (I/R). Nesfatin-1 significantly increased LVP, +max (dp/dt), -max (dp/dt) and HR in comparison with I/R group. This was associated with a significant decrease in LDH and CK-MB levels, a significant increase in SOD level and a significant decrease in MDA and CRP levels. Moreover, Nesfatin-1 caused a significant decrease in percentage of necrotic tissue to the whole left ventricular mass. Regarding group II, no significant changes were detected in all parameters except for significant increase in SOD level and significant decrease in CRP level. Conclusion: Nesfatin-1 protects against ischemia/reperfusion injury in vitro through its antioxidant and anti-inflammatory properties by limiting the infarction area, only if given as a post conditioning factor after I/R. Those results open the way to include Nesfatin-1 among the strategies for management of cardiac infarction during reperfusion.