Objective: To observe the treatment and it's mechanisms of rHu-EPO on acute myocardial infarction of SD rats in vitro and vivo.
Methods: Cardiomyocytes were isolated from neonatal Sprague-Dawley rats. Hypoxia condition and oxidative stress were used to induce apoptosis. rHu-EPO was added to the culture system. Apoptosis was assessed by using Hoechst 33258 dyeing. Apoptosis index (AI) was then calculated. Thirty two rats were divided into three groups including sham operation group (Sham), acute myocardial infarction group (MI) and treated group (MI + EPO). Acute myocardial infarction model was made by ligating the anterior descending coronary artery. rHu-EPO was administered i.p. in MI + EPO group at the dose of 5000 units/kg of body weight immediately after the ligation and the next six days. At the fourteenth day all animals underwent hemodynamic measurements and then executed, the samples were examined with hematoxylin and eosin (HE) stain, immunohistochemistry technique (Bcl-2, Bax) and TdT-mediated dUTP nick end labeling (TUNEL) dyeing.
Results: rHu-EPO significantly down-regulated the apoptosis of cardiomyocytes which underwent hypoxia or oxidative stress. In vivo experiment rHu-EPO protected the hemodynamic function of the rats from myocardial infarction and down-regulated the ratio of the positive cells for TUNEL and Bax. The ratio of the positive cells for Bcl-2 was up-regulated by rHu-EPO.
Conclusion: These findings suggested rHu-EPO improve myocardial infarction by attenuating apoptosis. Potential mechanism is to up-regulated Bcl-2 expression and down-regulated Bax expression.