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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

Expression of apoptotic myocardial cells in non-infarcted zones (NIZ) detected by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick end-labeling (TUNEL) staining (×200). (A) Sham, (B) myocardial infarction and (C) Qili qiangxin groups.
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f3-etm-0-0-2759: Expression of apoptotic myocardial cells in non-infarcted zones (NIZ) detected by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick end-labeling (TUNEL) staining (×200). (A) Sham, (B) myocardial infarction and (C) Qili qiangxin groups.

Mentions: The apoptotic cardiomyocytes were mainly distributed in the border zones of the infarction area (Fig. 3). The AI was markedly higher (P<0.01) in the MI and Qili qiangxin groups, when compared to the sham group (Table I). However, the AI in the Qili qiangxin group was significantly lower than that in the MI group (P<0.01).


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)

Expression of apoptotic myocardial cells in non-infarcted zones (NIZ) detected by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick end-labeling (TUNEL) staining (×200). (A) Sham, (B) myocardial infarction and (C) Qili qiangxin groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f3-etm-0-0-2759: Expression of apoptotic myocardial cells in non-infarcted zones (NIZ) detected by terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick end-labeling (TUNEL) staining (×200). (A) Sham, (B) myocardial infarction and (C) Qili qiangxin groups.
Mentions: The apoptotic cardiomyocytes were mainly distributed in the border zones of the infarction area (Fig. 3). The AI was markedly higher (P<0.01) in the MI and Qili qiangxin groups, when compared to the sham group (Table I). However, the AI in the Qili qiangxin group was significantly lower than that in the MI group (P<0.01).

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