Minocycline improves cardiac function after myocardial infarction in rats by inhibiting activation of PARP-1

To investigate whether Minocycline can protect myocardial cells after myocardial infarction and improve myocardial remodeling through inhibiting PARP-1 activity, thus improving cardiac function. 50 male Wistar rats aged 4 months were used to establish the myocardial infarction model. The experimental rats underwent the echocardiography at 3d, 14d and 28d after operation. After 28days, the rats were executed and the myocardial tissues in the infarct-related zone were treated with immumohistochemical staining and molecular biology detection. Our study found Minocycline could improve the cardiac function of rats after myocardial infarction. TUNEL results showed that Minocycline could reduce the apoptosis of myocardial cells after myocardial infarction. Western blotting results showed that Minocycline reduced the expressions of apoptotic proteins. Immunohistochemistry and Western blotting showed that Minocycline reduced the expressions of inflammatory factors, NF-κB and IL-1β, etc., in myocardial cells after myocardial infarction. Besides, it was found in further study that Minocycline could inhibit the PARP-1 activity after myocardial ischemic necrosis. In conclusion, Myocardial remodeling occurs after myocardial infarction, affecting the cardiac function. Minocycline can inhibit the activity of apoptosis and inflammatory factors, reduce the apoptosis, alleviate the inflammation and improve the ventricular remodeling through inhibiting PARP-1, thus protecting the cardiac function.