2018BMC Cardiovascular DisordersOpen access

Effects of procyanidin on cardiomyocyte apoptosis after myocardial ischemia reperfusion in rats

Dan Liu

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Abstract

BACKGROUND: This study is aimed at investigating the effects of procyanidin on cardiomyocyte apoptosis of myocardial ischemia/reperfusion (I/R) injury in rats. METHODS: Sprague-Dawley rats were randomly assigned into four groups: control group (normal saline), ischemic group (normal saline), procyanidin low-dose group (procyanidin 50 mg/kg/day) and procyanidin high-dose group (procyanidin 100 mg/kg/day) by intragastric administration for 2 weeks. After last administration, myocardial I/R model was induced by ligating left anterior descending artery for 30 min followed by 120 min of perfusion. The activity of serum creatine kinase mb isoenzyme (CK-MB) was detected after experiment. The content of reactive oxygen species (ROS) was determined by ROS fluorescent probe dihydroethidium; the expressions of p53, Caspase-9, Caspase-3, Bcl-2 and Bax were determined by western blotting; myocardial apoptosis was measured by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. RESULTS: Compared with control group, the contents of serum CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax increased significantly in ischemic group, the Bcl-2 expression, Bcl-2/Bax ratio decreased and the cardiomyocyte apoptosis index increased (p < 0.05); compared with ischemic group, the content of CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax decreased, the Bcl-2 expression, Bcl-2/Bax ratio increased and the cardiomyocyte apoptosis index decreased in procyanidin group (p < 0.05). CONCLUSIONS: Procyanidin can reduce cardiomyocyte apoptosis after I/R. This beneficial effect is partially dependant on decreased ROS, p53, Caspase-9, Caspase-3 and Bax, as well as increased Bcl-2 and Bcl-2/Bax ratio.

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BACKGROUND: This study is aimed at investigating the effects of procyanidin on cardiomyocyte apoptosis of myocardial ischemia/reperfusion (I/R) injury in rats. METHODS: Sprague-Dawley rats were randomly assigned into four groups: control group (normal saline), ischemic group (normal saline), procyanidin low-dose group (procyanidin 50 mg/kg/day) and procyanidin high-dose group (procyanidin 100 mg/kg/day) by intragastric administration for 2 weeks. After last administration, myocardial I/R model was induced by ligating left anterior descending artery for 30 min followed by 120 min of perfusion. The activity of serum creatine kinase mb isoenzyme (CK-MB) was detected after experiment. The content of reactive oxygen species (ROS) was determined by ROS fluorescent probe dihydroethidium; the expressions of p53, Caspase-9, Caspase-3, Bcl-2 and Bax were determined by western blotting; myocardial apoptosis was measured by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. RESULTS: Compared with control group, the contents of serum CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax increased significantly in ischemic group, the Bcl-2 expression, Bcl-2/Bax ratio decreased and the cardiomyocyte apoptosis index increased (p < 0.05); compared with ischemic group, the content of CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax decreased, the Bcl-2 expression, Bcl-2/Bax ratio increased and the cardiomyocyte apoptosis index decreased in procyanidin group (p < 0.05). CONCLUSIONS: Procyanidin can reduce cardiomyocyte apoptosis after I/R. This beneficial effect is partially dependant on decreased ROS, p53, Caspase-9, Caspase-3 and Bax, as well as increased Bcl-2 and Bcl-2/Bax ratio.

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Available abstract

BACKGROUND: This study is aimed at investigating the effects of procyanidin on cardiomyocyte apoptosis of myocardial ischemia/reperfusion (I/R) injury in rats. METHODS: Sprague-Dawley rats were randomly assigned into four groups: control group (normal saline), ischemic group (normal saline), procyanidin low-dose group (procyanidin 50 mg/kg/day) and procyanidin high-dose group (procyanidin 100 mg/kg/day) by intragastric administration for 2 weeks. After last administration, myocardial I/R model was induced by ligating left anterior descending artery for 30 min followed by 120 min of perfusion. The activity of serum creatine kinase mb isoenzyme (CK-MB) was detected after experiment. The content of reactive oxygen species (ROS) was determined by ROS fluorescent probe dihydroethidium; the expressions of p53, Caspase-9, Caspase-3, Bcl-2 and Bax were determined by western blotting; myocardial apoptosis was measured by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. RESULTS: Compared with control group, the contents of serum CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax increased significantly in ischemic group, the Bcl-2 expression, Bcl-2/Bax ratio decreased and the cardiomyocyte apoptosis index increased (p < 0.05); compared with ischemic group, the content of CK-MB, ROS, the expressions of p53, Caspase-9, Caspase-3 and Bax decreased, the Bcl-2 expression, Bcl-2/Bax ratio increased and the cardiomyocyte apoptosis index decreased in procyanidin group (p < 0.05). CONCLUSIONS: Procyanidin can reduce cardiomyocyte apoptosis after I/R. This beneficial effect is partially dependant on decreased ROS, p53, Caspase-9, Caspase-3 and Bax, as well as increased Bcl-2 and Bcl-2/Bax ratio.

Key concepts: Apoptosis, Proanthocyanidin, Caspase 3, Ischemia, Saline, Terminal deoxynucleotidyl transferase, Creatine kinase, Chemistry

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