Apigenin attenuates acute myocardial infarction of rats via the inhibitions of matrix metalloprotease-9 and inflammatory reactions.

Acute myocardial infarction (AMI) is the myocardial necrosis caused by coronary artery acute and persistent ischemia and hypoxia. Matrix metalloprotease-9 (MMP-9) plays an important role in a series of process of occurrence and development of AMI. Inflammatory reaction plays the key role in all kinds of damage factors in AMI. Apigenin (API) has effectively restrained the activity of MMP-9, anti-inflammatory and hepatic fat oxidizing properties. API significantly improved AMI of rats through inhibiting MMP-9 and inflammatory reactions in a few recent studies. Our investigation detected the infarct size of AMI rats, casein kinase (CK), the MB isoenzyme of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) activities in AMI rats were also analyzed with commercial kits. Additionally, Nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) levels of whole bloods of AMI rats were also detected using commercial kits. Next, MMP-9 protein of cardiac in AMI rats was measured with gelatin zymography assays. Finally, caspase-3 and caspase-9 activities in AMI rats were analyzed with commercial kits. In the present study, our work indicated API might significantly reduce the infarction size of AMI rat. It was shown that the treatment of API could decrease the expression of MMP-9 level and reduce the activities of NF-κB, TNF-α, IL-1β and IL-6 in AMI rats. Next, API treatment could reduce caspase-3 and caspase-9 activities and decrease cellular apoptosis of AMI rats. Our findings concluded that API ameliorates acute myocardial infarction of rats via inhibiting MMP-9 and inflammatory reactions.