2017Zhonghua shiyan waike zazhiRequires access

The protective effects of atorvastatin preconditioning on ischemia-reperfusion injury in rats

Ximing Wang, Yanxia Zhang, Haibin Yu, Chengshan Gao, Hongshan Wang, Genshang Zhao

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Abstract

Objective To investigate the protective effect of atorvastatin precondtioning on cardiomyocytes following myocardial ischemia-reperfusion injury (MIRI) in rats. Methods Forty health male Sprague-Dawley rats were randomly divided into four groups: sham group (group A), ischemia-reperfusion group (group B), atorvastatin preconditioning groups (group C, 20 mg/day; group D, 40 mg/day). The MIRI model of rats in vivo had been established successfully. Hematoxylin-eosin staining (HE) method was used to identify the pathologic changes of myocardial tissue. The mRNA expression level of B-cell lymphoma/leukemia-2 (bcl-2) and B cell lymphoma/leukemia-2 associated X protein (bax) was determined by the methods of reverse transcriptase-polymerase chain reaction (RT-PCR). The activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured. Results As compared with the group A, obvious myocardial ischemia and myocardial infarction area were seen in group B, C and D. As compared with the group B [1.67±0.31, (32.95±4.51) U/mg pro], the mRNA expression level of bcl-2 (3.31±0.27, t=2.231, P=0.028; 4.93±0.53, t=2.125, P=0.034) and the activity of SOD [(59.81±6.02) U/mg pro, t=3.510, P=0.000; (68.78±4.37) U/mg pro, t=4.439, P=0.000] was increased. The level of bax (3.28±0.31, t=3.630, P=0.000; 2.06±0.41, t=4.039, P=0.000) and the content of MDA [(4.63±0.27) nmol/mg pro, t=2.151, P=0.031; (3.55±0.57) nmol/mg pro, t=2.445, P=0.024] were significantly decreased in the different preconditioning groups compared with the group B [5.70±0.42, (6.77±0.44) nmol/mg pro]. Conclusion Atorvastatin pretreatment can significantly increase antioxidant enzyme activity, inhibit the lipid peroxidation injury, decrease the apoptosis of myocardium induced by MIRI, and protect the myocardium of rats from ischemic reperfusion injury. Key words: Atorvastatin; Myocardial ischemia; Reperfusion injury; Apoptosis

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Objective To investigate the protective effect of atorvastatin precondtioning on cardiomyocytes following myocardial ischemia-reperfusion injury (MIRI) in rats. Methods Forty health male Sprague-Dawley rats were randomly divided into four groups: sham group (group A), ischemia-reperfusion group (group B), atorvastatin preconditioning groups (group C, 20 mg/day; group D, 40 mg/day). The MIRI model of rats in vivo had been established successfully. Hematoxylin-eosin staining (HE) method was used to identify the pathologic changes of myocardial tissue. The mRNA expression level of B-cell lymphoma/leukemia-2 (bcl-2) and B cell lymphoma/leukemia-2 associated X protein (bax) was determined by the methods of reverse transcriptase-polymerase chain reaction (RT-PCR). The activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured. Results As compared with the group A, obvious myocardial ischemia and myocardial infarction area were seen in group B, C and D. As compared with the group B [1.67±0.31, (32.95±4.51) U/mg pro], the mRNA expression level of bcl-2 (3.31±0.27, t=2.231, P=0.028; 4.93±0.53, t=2.125, P=0.034) and the activity of SOD [(59.81±6.02) U/mg pro, t=3.510, P=0.000; (68.78±4.37) U/mg pro, t=4.439, P=0.000] was increased. The level of bax (3.28±0.31, t=3.630, P=0.000; 2.06±0.41, t=4.039, P=0.000) and the content of MDA [(4.63±0.27) nmol/mg pro, t=2.151, P=0.031; (3.55±0.57) nmol/mg pro, t=2.445, P=0.024] were significantly decreased in the different preconditioning groups compared with the group B [5.70±0.42, (6.77±0.44) nmol/mg pro]. Conclusion Atorvastatin pretreatment can significantly increase antioxidant enzyme activity, inhibit the lipid peroxidation injury, decrease the apoptosis of myocardium induced by MIRI, and protect the myocardium of rats from ischemic reperfusion injury. Key words: Atorvastatin; Myocardial ischemia; Reperfusion injury; Apoptosis

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Available abstract

Objective To investigate the protective effect of atorvastatin precondtioning on cardiomyocytes following myocardial ischemia-reperfusion injury (MIRI) in rats. Methods Forty health male Sprague-Dawley rats were randomly divided into four groups: sham group (group A), ischemia-reperfusion group (group B), atorvastatin preconditioning groups (group C, 20 mg/day; group D, 40 mg/day). The MIRI model of rats in vivo had been established successfully. Hematoxylin-eosin staining (HE) method was used to identify the pathologic changes of myocardial tissue. The mRNA expression level of B-cell lymphoma/leukemia-2 (bcl-2) and B cell lymphoma/leukemia-2 associated X protein (bax) was determined by the methods of reverse transcriptase-polymerase chain reaction (RT-PCR). The activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured. Results As compared with the group A, obvious myocardial ischemia and myocardial infarction area were seen in group B, C and D. As compared with the group B [1.67±0.31, (32.95±4.51) U/mg pro], the mRNA expression level of bcl-2 (3.31±0.27, t=2.231, P=0.028; 4.93±0.53, t=2.125, P=0.034) and the activity of SOD [(59.81±6.02) U/mg pro, t=3.510, P=0.000; (68.78±4.37) U/mg pro, t=4.439, P=0.000] was increased. The level of bax (3.28±0.31, t=3.630, P=0.000; 2.06±0.41, t=4.039, P=0.000) and the content of MDA [(4.63±0.27) nmol/mg pro, t=2.151, P=0.031; (3.55±0.57) nmol/mg pro, t=2.445, P=0.024] were significantly decreased in the different preconditioning groups compared with the group B [5.70±0.42, (6.77±0.44) nmol/mg pro]. Conclusion Atorvastatin pretreatment can significantly increase antioxidant enzyme activity, inhibit the lipid peroxidation injury, decrease the apoptosis of myocardium induced by MIRI, and protect the myocardium of rats from ischemic reperfusion injury. Key words: Atorvastatin; Myocardial ischemia; Reperfusion injury; Apoptosis

Key concepts: Malondialdehyde, Reperfusion injury, Atorvastatin, Medicine, Superoxide dismutase, Ischemia, H&E stain, Myocardial infarction

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