CORM2 protects from myocardial ischemia reperfusioninjury via modulation of the inflammatory response and apoptosis
Background: Myocardial ischemia is one of the major clinical problems in the world. There are two forms of the cell injury occur during myocardial ischemia, which are necrosis and apoptosis. Reperfusion is very important to maintain the viability of the myocardial cells, but in the other hand reperfusion not free from hazardous effects and it is usually associated with what is called ischemia reperfusion injury. Objective: This study was undertaken to assess the possible protective potential of Carbone monoxide releasing molecule-2 (CORM2) in regional myocardial ischemia reperfusion injury and apoptosis in male rats. Methods: Twenty four adult male Swiss albino rats were divided into four groups (six rats per group). Sham , in a uniform manner, surgical procedure was done for the rats in all groups, and in this group there was no ligation for (LAD). Control group, rats were subjected for ligation of LAD for 30minutes then 3hr reperfusion. vehicle group, rats were subjected for ligation of LAD for 30minutes then 3hr reperfusion and received 0.5%DMSO before reperfusion time. Treatment group: reperfusion lasted for 3 hours after LAD ligation for half an hour, treatment with CORM2 at reperfusion time (8mg/kg I.V via the tail vein) have done to all rats. Results: At the end of reperfusion animals sacrificed and cardiac TNF-α, IL-1β ,IL-6, ssDNA and plasma troponin I (cTnI) were measured. It has been found that CORM2 treated group showed a significant reduction (P< 0.05) in cardiac TNF-α, IL-1β, IL-6, ssDNA and plasma cardiac troponin I (cTnI) compared with the control group. Histopathological study found that treatment with CORM2 significantly (P<0.05) reduce the myocardial injury compared with the control group Conclusion: CORM2 lead to reduction in regional myocardial ischemia reperfusion injury and apoptosis during ischemia via interfering with inflammatory pathway.
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