Traditional Chinese medicine Qili qiangxin inhibits cardiomyocyte apoptosis in rats following myocardial infarction

• Published in: Experimental and therapeutic medicine 2015-11, Vol.10 (5), p.1817-1823
• Main Authors: XIAO, JUN, DENG, SONG-BAI, SHE, QIANG, LI, JUN, KAO, GUO-YING, WANG, JUN-SHENG, MA, YU
• Format: Article
• Language: English
• Subjects: Apoptosis; Binding sites; Cardiomyocytes; Care and treatment; Chinese medicine; Coronary vessels; Deoxyribonucleic acid; DNA; Enzymes; FDA approval; Free radicals; Health aspects; Heart attack; Heart attacks; Heart cells; Heart failure; Kinases; myocardial infarction; Ostomy; Prevention; Qili qiangxin; Reactive oxygen species; Rodents; Veins & arteries; Ventilators; xanthine oxidase
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2015.2759

The aim of the present study was to examine the effect of the traditional Chinese medicine Qili qiangxin on cardiomyocyte apoptosis following myocardial infarction (MI) in a rat model. MI was induced in rats by ligation of the anterior descending coronary artery. Survivors were randomly divided into the sham operation, MI, and Qili qiangxin groups (4 g/kg per day). After 28 days, infarction size was measured. In the non-infarcted zones (NIZ), the apoptotic index (AI) was measured by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick-end labeling (TUNEL). Expression of Fas was detected by immunohistochemistry, and the expression of xanthine oxidase (XO) and caspase-3 by western blot analysis. In addition, the XO and ·O2−, ·OH-scavenging activity of myocardial tissue in NIZ was measured by colorimetry. Compared to the MI group, AI and the expression of Fas and caspase-3 were significantly decreased in NIZ. The activity of XO was also considerably reduced while ·O2− and ·OH-scavenging activity was significantly increased in the Qili qiangxin group. Ventricular remodeling was attenuated but there were no significant differences in infarct size (IS) or XO expression levels between the Qili qiangxin and MI groups. In conclusion, the results suggest that Qili qiangxin may inhibit cardiomyocyte apoptosis in NIZ in rats. The potential mechanism involved may be associated with its ability to reduce reactive oxygen species (ROS) and to depress the expression of Fas and caspase-3.