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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

Representative M-mode echocardiograms of the left ventricle in the parasternal short-axis view of 28 days post-myocardial infarction (MI): (A) sham group; (B) MI group and (C) Qiliqiangxin group.
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f1-etm-0-0-2759: Representative M-mode echocardiograms of the left ventricle in the parasternal short-axis view of 28 days post-myocardial infarction (MI): (A) sham group; (B) MI group and (C) Qiliqiangxin group.

Mentions: After 28 days, 6 rats in the MI group and 1 rat in the Qili qiangxin group died. The rats in the sham group survived. Compared to the sham group, LVEDD was increased and FS and EF were significantly decreased in the MI group (P<0.01). However, compared to the MI group LVEDD was decreased, and FS and EF were significantly increased in the Qili qiangxin group (P<0.01). Although IS was smaller in the Qili qiangxin group than that in the MI group, the difference was not statistically significant (P>0.05), (Table I, Figs. 1 and 2). No infarct was detected in the sham group since none of the rats underwent ligation of the coronary artery.


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)

Representative M-mode echocardiograms of the left ventricle in the parasternal short-axis view of 28 days post-myocardial infarction (MI): (A) sham group; (B) MI group and (C) Qiliqiangxin group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-etm-0-0-2759: Representative M-mode echocardiograms of the left ventricle in the parasternal short-axis view of 28 days post-myocardial infarction (MI): (A) sham group; (B) MI group and (C) Qiliqiangxin group.
Mentions: After 28 days, 6 rats in the MI group and 1 rat in the Qili qiangxin group died. The rats in the sham group survived. Compared to the sham group, LVEDD was increased and FS and EF were significantly decreased in the MI group (P<0.01). However, compared to the MI group LVEDD was decreased, and FS and EF were significantly increased in the Qili qiangxin group (P<0.01). Although IS was smaller in the Qili qiangxin group than that in the MI group, the difference was not statistically significant (P>0.05), (Table I, Figs. 1 and 2). No infarct was detected in the sham group since none of the rats underwent ligation of the coronary artery.

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