Huoxue anxin recipe alleviated peroxidation damage of acute myocardial infarction rats by regulating iNOS/eNOS imbalance: an experimental research / 中国中西医结合杂志

ABSTRACT

<p><b>OBJECTIVE</b>To study the protective mechanism of Huoxue Anxin Recipe (HAR) on peroxidation damage of acute myocardial infarction (AMI) rats.</p><p><b>METHODS</b>The AMI rat model was established by occluding the left anterior descending coronary artery. Compound Danshen Dripping Pill (CDDP) was used as the positive control. CDDP and HAR were administered to rats for 7 successive days since modeling. The heart function was detected using color Doppler echocardiography. Activities of induced nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), total superoxide dismutase (tSOD) activity, and contents of malondialdehyde (MDA) were detected by ultraviolet spectrophotometer method.</p><p><b>RESULTS</b>Compared with the sham-operation group, ejection fraction (EF) and fraction shortening (FS) rate significantly decreased in the model group (P < 0.01). Compared with the model group, EF and FS rate significantly increased in the HAR group, showing statistical difference (P < 0.05). There was no statistical difference in activities of serum iNOS, eNOS, or tSOD among all groups (P > 0.05). Compared with the sham-operation group, iNOS activities and MDA contents significantly increased in the myocardial tissue of the model group (P < 0.01), activities of eNOS and tSOD significant decreased (P < 0.01). Compared with the model group, iNOS activities in the myocardial tissue, MDA contents both in serum and the myocardial tissue significantly decreased (P < 0.05), activities of eNOS and tSOD significantly increased in the HAR group (P < 0.05). There was no statistical difference in each index between the CDDP group and the HAR group (P > 0.05).</p><p><b>CONCLUSIONS</b>HAR could significantly improve cardiac functions of AMI rats. Its roles might be associated with regulating imbalanced iNOS/eNOS expressions and alleviating peroxidation damage of the myocardial tissue.</p>