Protective effect of nicorandil postconditioning on myocardium of rats with myocardial ischemia-reperfusion injury
Keqiang Zhang
Abstract
Keqiang Zhang
Abstract
Objective To explore the protective effect of nicorandil postconditioning on myocardium of rats with myocardial ischemia-reperfusion injury(MIRI) in rats and to discuss its mechanism.Methods 26 SD rats were divided into control group(n=8),isoproterenol(ISO) group(n=8) and nicorandil postconditioning group(n=10).The rats in ISO group were injected intraperitoneally with isoproterenol(5 mg·kg-1)at an interval of 24 h for 3 d;the rats in control group only received an injection of same amount of saline;the rats in nicorandil postconditioning group were injected intravenously with nicorandil(1 mg·kg-1) 1 h after ISO injection once a day,lasting for 3 d.The rats were killed 24 h after the third injection of ISO.The activities of serum creatine kinase(CK) and lactate dehydrogenase(LDH) of rats in various groups were detected;the histopathological changes of myocardium of rats in various groups were observed by routine HE staining;the expressions of Caspase-3 protein were determined by immunohistochemistry;the apoptosis of cardiocytes of rats in various groups was analyzed by TUNEL staining.Results There were no significant differences in the activites of serum CK and LDH between nicorandil postconditioning group and control group(P0.05),but the activities of CK and LDH in control and nicorandil postconditioning groups were lower than those in ISO group(P0.05).The HE staining results showed local degeneration,necrosis and inflammation in ISO group,but slightly necrosis and inflammation in nicorandil postconditioning group and no pathological changes in control group.Immunohistochemistry staining showed that Caspase-3 was positive in cardiocyte plasma in ISO group;however,there were no Caspase-3 expression in control and nicorandil postconditioning groups.The apoptosis index(AI) in nicorandil postconditioning group was significantly decreased compared with ISO group(P0.01).Conclusion Nicorandil can attenuate MIRI of rats,and its mechanism may be related to inhibiting Caspase-3 pathway and decreasing the cardiocyte apoptosis.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To explore the protective effect of nicorandil postconditioning on myocardium of rats with myocardial ischemia-reperfusion injury(MIRI) in rats and to discuss its mechanism.Methods 26 SD rats were divided into control group(n=8),isoproterenol(ISO) group(n=8) and nicorandil postconditioning group(n=10).The rats in ISO group were injected intraperitoneally with isoproterenol(5 mg·kg-1)at an interval of 24 h for 3 d;the rats in control group only received an injection of same amount of saline;the rats in nicorandil postconditioning group were injected intravenously with nicorandil(1 mg·kg-1) 1 h after ISO injection once a day,lasting for 3 d.The rats were killed 24 h after the third injection of ISO.The activities of serum creatine kinase(CK) and lactate dehydrogenase(LDH) of rats in various groups were detected;the histopathological changes of myocardium of rats in various groups were observed by routine HE staining;the expressions of Caspase-3 protein were determined by immunohistochemistry;the apoptosis of cardiocytes of rats in various groups was analyzed by TUNEL staining.Results There were no significant differences in the activites of serum CK and LDH between nicorandil postconditioning group and control group(P0.05),but the activities of CK and LDH in control and nicorandil postconditioning groups were lower than those in ISO group(P0.05).The HE staining results showed local degeneration,necrosis and inflammation in ISO group,but slightly necrosis and inflammation in nicorandil postconditioning group and no pathological changes in control group.Immunohistochemistry staining showed that Caspase-3 was positive in cardiocyte plasma in ISO group;however,there were no Caspase-3 expression in control and nicorandil postconditioning groups.The apoptosis index(AI) in nicorandil postconditioning group was significantly decreased compared with ISO group(P0.01).Conclusion Nicorandil can attenuate MIRI of rats,and its mechanism may be related to inhibiting Caspase-3 pathway and decreasing the cardiocyte apoptosis.
Key concepts: Nicorandil, Lactate dehydrogenase, Creatine kinase, Medicine, H&E stain, TUNEL assay, Necrosis, Ischemia