2013Unpublished venueRequires access

Protection of postconditioning with nicorandil on myocardial ischemia/reperfusion injury

Keqiang Zhang

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Abstract

Objective To explore the mechanism of protection of postconditioning with nicorandil on myocardial ischemia /reperfusion(I/R) injury in rats.Methods Twenty-six SD rats were randomly divided into control group(8 rats),isoproterenol(ISO) group(8 rats) and nicorandil postconditioning group(10 rats).ISO(5mg/kg) was injected intraperitoneally to ISO group and nicorandil postconditioning group once daily for 3 days.For nicorandil group,rats were injected via tail vein with nicorandil(1mg/kg) 1 hour after ISO injection once daily for 3 days.While same amount of physiological saline was injected to control group rats.Rats from 3 groups were sacrificed 24 hours after the 3rd day injection.Serum cardiac troponin I(cTnI) was measured,and the expressions of potassium ion channel protein kir6.2,voltage-dependent anion channel(VDAC) and Il10 were detected and stained by nitrotyrosine immunohistochemistry approach.Results Serum cTnI level of nicorandil group was significantly lower than that of ISO group(P﹤0.01).Comparing to control group,the expression of Kir6.2 was significantly lower in ISO group while was higher in nicorandil group.No differences were found in expression of VDAC among these three groups.Big amount of nitrotyrosine was observed in cytoplasm of cardiocytes in ISO group and no nitrotyrosine was found in the other two groups.The expression of I1-10 was significant higher in nicorandil group than that in ISO and control group.Conclusions Nicorandil postconditioning attenuates myocardial ischemia /reperfusion injury,possibly by inhibiting free radicals generation and inflammatory response via opening potassium channels.

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Objective To explore the mechanism of protection of postconditioning with nicorandil on myocardial ischemia /reperfusion(I/R) injury in rats.Methods Twenty-six SD rats were randomly divided into control group(8 rats),isoproterenol(ISO) group(8 rats) and nicorandil postconditioning group(10 rats).ISO(5mg/kg) was injected intraperitoneally to ISO group and nicorandil postconditioning group once daily for 3 days.For nicorandil group,rats were injected via tail vein with nicorandil(1mg/kg) 1 hour after ISO injection once daily for 3 days.While same amount of physiological saline was injected to control group rats.Rats from 3 groups were sacrificed 24 hours after the 3rd day injection.Serum cardiac troponin I(cTnI) was measured,and the expressions of potassium ion channel protein kir6.2,voltage-dependent anion channel(VDAC) and Il10 were detected and stained by nitrotyrosine immunohistochemistry approach.Results Serum cTnI level of nicorandil group was significantly lower than that of ISO group(P﹤0.01).Comparing to control group,the expression of Kir6.2 was significantly lower in ISO group while was higher in nicorandil group.No differences were found in expression of VDAC among these three groups.Big amount of nitrotyrosine was observed in cytoplasm of cardiocytes in ISO group and no nitrotyrosine was found in the other two groups.The expression of I1-10 was significant higher in nicorandil group than that in ISO and control group.Conclusions Nicorandil postconditioning attenuates myocardial ischemia /reperfusion injury,possibly by inhibiting free radicals generation and inflammatory response via opening potassium channels.

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Available abstract

Objective To explore the mechanism of protection of postconditioning with nicorandil on myocardial ischemia /reperfusion(I/R) injury in rats.Methods Twenty-six SD rats were randomly divided into control group(8 rats),isoproterenol(ISO) group(8 rats) and nicorandil postconditioning group(10 rats).ISO(5mg/kg) was injected intraperitoneally to ISO group and nicorandil postconditioning group once daily for 3 days.For nicorandil group,rats were injected via tail vein with nicorandil(1mg/kg) 1 hour after ISO injection once daily for 3 days.While same amount of physiological saline was injected to control group rats.Rats from 3 groups were sacrificed 24 hours after the 3rd day injection.Serum cardiac troponin I(cTnI) was measured,and the expressions of potassium ion channel protein kir6.2,voltage-dependent anion channel(VDAC) and Il10 were detected and stained by nitrotyrosine immunohistochemistry approach.Results Serum cTnI level of nicorandil group was significantly lower than that of ISO group(P﹤0.01).Comparing to control group,the expression of Kir6.2 was significantly lower in ISO group while was higher in nicorandil group.No differences were found in expression of VDAC among these three groups.Big amount of nitrotyrosine was observed in cytoplasm of cardiocytes in ISO group and no nitrotyrosine was found in the other two groups.The expression of I1-10 was significant higher in nicorandil group than that in ISO and control group.Conclusions Nicorandil postconditioning attenuates myocardial ischemia /reperfusion injury,possibly by inhibiting free radicals generation and inflammatory response via opening potassium channels.

Key concepts: Nicorandil, Nitrotyrosine, Troponin I, Medicine, Reperfusion injury, Ischemia, Internal medicine, Saline

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