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

Xiao J, Deng SB, She Q, Li J, Kao GY, Wang JS, Ma YU - Exp Ther Med (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Chongqing Medical Emergency Center, Chongqing 400014, P.R. China.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Agarose gel electrophoresis of myocardial deoxyribonucleic acid (DNA) in non-infarcted zones (NIZ): M, DNA marker; 1, myocardial infarction group; 2, Qiliqiangxin group; 3, sham group.
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f4-etm-0-0-2759: Agarose gel electrophoresis of myocardial deoxyribonucleic acid (DNA) in non-infarcted zones (NIZ): M, DNA marker; 1, myocardial infarction group; 2, Qiliqiangxin group; 3, sham group.

Mentions: Following agarose gel electrophoresis, the myocardial tissue DNA of the sham group exhibited a late band close to the sample well, which was recognized as the normal band pattern for cardiomyocyte DNA. The distribution of DNA fragments in the MI group was dispersed and a typical DNA ladder was observed while the relatively minor dispersion of the DNA fragments was detected in the Qili qiangxin group which made the DNA ladder disappear (Fig. 4).


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

Xiao J, Deng SB, She Q, Li J, Kao GY, Wang JS, Ma YU - Exp Ther Med (2015)

Agarose gel electrophoresis of myocardial deoxyribonucleic acid (DNA) in non-infarcted zones (NIZ): M, DNA marker; 1, myocardial infarction group; 2, Qiliqiangxin group; 3, sham group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4665999&req=5

f4-etm-0-0-2759: Agarose gel electrophoresis of myocardial deoxyribonucleic acid (DNA) in non-infarcted zones (NIZ): M, DNA marker; 1, myocardial infarction group; 2, Qiliqiangxin group; 3, sham group.
Mentions: Following agarose gel electrophoresis, the myocardial tissue DNA of the sham group exhibited a late band close to the sample well, which was recognized as the normal band pattern for cardiomyocyte DNA. The distribution of DNA fragments in the MI group was dispersed and a typical DNA ladder was observed while the relatively minor dispersion of the DNA fragments was detected in the Qili qiangxin group which made the DNA ladder disappear (Fig. 4).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Chongqing Medical Emergency Center, Chongqing 400014, P.R. China.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus