RESUMO
Objective:To investigate the protective effect and mechanism of isorhamnetin on myocardial injury in rats with acute myocardial infarction (AMI).Methods:The AMI rat model was established by coronary artery left anterior descending ligation. The SD rats were divided into sham-operated group, model group, Fasudil group (30 mg/kg) and low-, medium-, and high-dose (25, 50, 100 mg/kg) groups. Each group had 5 rats. They were administrated intragastric, once a day, and were treated for 14 d. Color Doppler ultrasonography was used to detect cardiac function by measuring left ventricular end-systolic diameter (LVESd), left ventricular end-diastolic diameter (LVEDd), and left ventricular long-axis shortening fraction (FS). Myocardial infarct size was detected by TCT staining. Superoxide dismutase (SOD), malondialdehyde (MDA), interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) levels in rat serum were detected by ELISA and TUNEL assay for the cardiomyocyte apoptosis index. Cysteinyl aspartate specific proteinase-3 (Caspase-3) activity in myocardial tissue was detected by the Caspase-3 activity assay kit, and the expression of Bcl-2 associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) proteins in myocardial tissue was detected by Western Blot.Results:Compared with the sham operation group, the FS, SOD content, and expression levels of Bcl-2 protein in the model group were significantly decreased (all P<0.05), and LVEDd, LVESd, myocardial infarct size, MDA content, IL-6 content, TNF-α content, IL-1β content, apoptosis index, Caspase-3 activity, and Bax protein expression level were significantly increased (all P<0.05). There was no significant difference between the low concentration of isorhamnetin and the model group (all P>0.05). However, the above changes caused by the construction model after treatment with Fasudil and medium- and high-concentrations of isorhamnetin significantly reversed (all P<0.05). Conclusions:Isorhamnetin can improve cardiac function and protect myocardial injury in AMI rats by reducing oxidative stress and inflammatory damage to cardiomyocytes and inhibiting cardiomyocyte apoptosis.