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.