Protective Effect of Cortex Fraxini on Heart Injury in a Rat Model of Myocardial Infarction

ABSTRACT Objectives：Myocardial infarction is caused by heart cell death in a region where coronary arteries supplying blood to the region are occluded. In the present study, we determined whether ethanol extract of Cortex fraxini (HY5053) could attenuate heart injury by inhibiting apoptosis. Methods：Improvement of survival of HepG2 cells, a human hepatocellular carcinoma cell line, and reduction of apoptosis under hypoxic conditions (3% O 2 ) were assessed by trypan blue staining and DNA fragmentation assay, respectively. To assess the impact of HY5053 on the hear t injury, Sprague-Dawley rats underwent 1 day of the left anterior descending coronary artery occlusion. HY5053 was given by intraperitoneal injection (200 mg/kg) 1 hr prior to the occlusion. Subsequently, the heart were harvested, excised into 4 slices, and the slices were stained with 2,3,5-triphenyl tetrazolium chloride. Finally , the extent of heart injury represented as ischemic index (%) was assessed. Results：Addition of HY5053 (400 ㎍/mL) into the culture medium for 1 day under ischemic conditions improved the cell survival by 50%, compared with control (0 ㎍/mL), conse quently delayed apoptosis in 6 hr difference. Also, HY5053 (200 mg/kg) reduced the ischemic index by 44%, com pared with control (0 mg/kg). Conclusions：These findings suggested that HY5053 attenuated myocardial infa rction by inhibiting apoptosis. Thus, Cortex fraxini could be developed as a novel cardioprotec tant to complement a currently available treatment, coronary angioplasty.Key words：Cortex fraxini, myocardial infarction, apoptosis, cardioprotect ant