P673CORM2 ameliorates myocardial ischemia /reperfusion injury via down regulation of apoptosis and inflammatory response

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Background:The importance of apoptosis in cell death following ischemia and reperfusion has been demonstrated in vivo rodent modelsA potential strategy to alleviate cardiac I/Ri is to exploit the potent anti-inflammatory and cytoprotective effects of carbon monoxide (CO) by application of so-called CO-releasing molecules (CORMs). Here, we assessed whether CO released from CORM-2 protects against cardiac I/Ri in a rat model.

Material and method: Rats were subjected to surgical induction of ischemia and reperfusion by ligation of the left interior descending artery (LAD) for 30minutes and 3hr reperfusion and received CORM2 or control vehicle, at the end of experiment the animals were sacrificed and blood sample taken to measure cardiac troponin I and cardiac section was taken to to measure TNF-α, IL-1β and IL-6.Further, cardiac section was taken to make histopathological study and other section to measure apoptosis cell by ssDNA apoptotic kit.

Result: Compared to sham group, the levels of cardiac TNF-α, IL-1β, IL-6,ssDNA and plasma level of cardiac troponin I (cTnI) increased in control group (p<0.05). Histological, all rats in control group showed significant (p<0.05) cardiac injury. CORM2 significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, IL-6,ssDNA and plasma level of (cTnI) compared to control and control vehicle (p<0.05). Morphologic analysis showed that CORM2 markedly improved (p<0.05) the severity of cardiac injury.

Conclusions: CORM2 may ameliorate regional myocardial ischemia reperfusion injury and apoptosis during ischemia via interfering with inflammatory pathway.

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