Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.
Bottom Line: Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment.Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration.Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05).
Affiliation: Heart Research Center, Chonnam National University Hospital, Gwangju, South Korea.Show MeSH
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Mentions: To investigate the role of 5AZ in MI, MI was induced by permanent ligation of the left anterior descending coronary artery in rats. To confirm whether the surgery was induced similar MI in all animals, infarct size was assessed at 24 hrs. Infarct size was similar in the two groups (Fig.4A). Then, 5AZ or saline was administered, and heart tissue was harvested 2 weeks after MI. Cardiac fibrosis was reduced to 8.14 ± 1.00% by 5AZ administration from 14.93 ± 2.98% (Fig.4B).
Affiliation: Heart Research Center, Chonnam National University Hospital, Gwangju, South Korea.