In the present study, the myocardial protective effects of
erythropoietin (EPO) by inhibition of the expression of
caspase-12 were investigated in a
myocardial infarction rat model. Thirty male SD rats were divided into three groups:
sham-operation group,
myocardial infarction group and EPO treatment group. The
myocardial infarction model was created by ligating the left anterior descending coronary artery. The EPO treatment group was established by injecting rh-EPO (1,000 IU/kg) intraperitoneally every day after the operation, and the other two groups were injected with
sodium chloride. Four weeks after induction of
myocardial infarction, the left ventricular diastolic pressure (LVDP) was tested by Langendorff apparatus and the pathological changes were analyzed by H&E staining.
Caspase-12 expression in the left ventricular myocardium was also measured by immunohistochemistry. Four weeks after induction of
myocardial infarction, the improvement in heart function in the EPO treatment group was more distinct compared to that of the
myocardial infarction group; LVDP was higher in the EPO treatment group compared to the
myocardial infarction group, but lower compared to the control group. H&E staining showed that the myocardial cells in the normal control group were aligned in order with a clear structure and were stained equably, while the myocardial cells in the
myocardial infarction model rats lined up in disorder with an augmented cell body appearing to have many granules and interstitial
fibrosis. Myocardial
fibrosis and disorder were improved in the EPO treatment group. The expression of
caspase-12 in the
myocardial infarction group was also increased compared to the EPO treatment group rats. The results suggest that EPO improves heart function in
myocardial infarction rats by down-regulating the expression of
caspase-12, which may protect the myocardium by abrogating endoplasmic reticulum stress-mediated cardiomyocyte apoptosis and improving heart function.