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

흰쥐를 이용한 심근경색모델에서 진피(秦皮)의 심장손상 보호효과

  • Lim, Sun-Ha (Departmet of Biochemistry, School of Medicine, Catholic University of Daegu) ;
  • Lee, Jong-Won (Departmet of Biochemistry, School of Medicine, Catholic University of Daegu)
  • 임선하 (대구가톨릭대학교 의과대학 생화학교실) ;
  • 이종원 (대구가톨릭대학교 의과대학 생화학교실)
  • Received : 2011.08.24
  • Accepted : 2011.12.16
  • Published : 2011.12.30

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 heart 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 ${\mu}g$/mL) into the culture medium for 1 day under ischemic conditions improved the cell survival by 50%, compared with control (0 ${\mu}g$/mL), consequently delayed apoptosis in 6 hr difference. Also, HY5053 (200 mg/kg) reduced the ischemic index by 44%, compared with control (0 mg/kg). Conclusions : These findings suggested that HY5053 attenuated myocardial infarction by inhibiting apoptosis. Thus, Cortex fraxini could be developed as a novel cardioprotectant to complement a currently available treatment, coronary angioplasty.

Keywords

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