2011Journal of Zhengzhou UniversityRequires access

Cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats

Shuangfeng Li

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Abstract

Aim:To observe the cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats and the possible mechanism.Methods:Thirty-two male SD rats were randomly divided into 4 groups:group sham,IR group(group IR),hydrogen sulfide treatment group(group H2S)and 5-HD+H2S group(group 5-HD).IR model was made by ligation of the anterior descending coronaryartery for 30 min followed by 120 min reperfusion.We observed myocardial ultrastructure under electron microscope and detected myocardial Bcl-2 and Bax protein by western blotting.Results:The expressions of Bcl-2 and Bax protein among 4 groups were different,there were obvious differences(F=31.937 and 11.681,P0.001).The expressions of Bcl-2 protein was higher and Bax protein was lower in group IR than in group H2S(P0.05);there was no significant difference in group IR and in group 5-HD(P0.05).Conclusion:Hydrogen sulfide protect myocardial function.Regulation of cell apoptosis and activating mitoKATP are the possible mechanisms.

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Aim:To observe the cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats and the possible mechanism.Methods:Thirty-two male SD rats were randomly divided into 4 groups:group sham,IR group(group IR),hydrogen sulfide treatment group(group H2S)and 5-HD+H2S group(group 5-HD).IR model was made by ligation of the anterior descending coronaryartery for 30 min followed by 120 min reperfusion.We observed myocardial ultrastructure under electron microscope and detected myocardial Bcl-2 and Bax protein by western blotting.Results:The expressions of Bcl-2 and Bax protein among 4 groups were different,there were obvious differences(F=31.937 and 11.681,P0.001).The expressions of Bcl-2 protein was higher and Bax protein was lower in group IR than in group H2S(P0.05);there was no significant difference in group IR and in group 5-HD(P0.05).Conclusion:Hydrogen sulfide protect myocardial function.Regulation of cell apoptosis and activating mitoKATP are the possible mechanisms.

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Available abstract

Aim:To observe the cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats and the possible mechanism.Methods:Thirty-two male SD rats were randomly divided into 4 groups:group sham,IR group(group IR),hydrogen sulfide treatment group(group H2S)and 5-HD+H2S group(group 5-HD).IR model was made by ligation of the anterior descending coronaryartery for 30 min followed by 120 min reperfusion.We observed myocardial ultrastructure under electron microscope and detected myocardial Bcl-2 and Bax protein by western blotting.Results:The expressions of Bcl-2 and Bax protein among 4 groups were different,there were obvious differences(F=31.937 and 11.681,P0.001).The expressions of Bcl-2 protein was higher and Bax protein was lower in group IR than in group H2S(P0.05);there was no significant difference in group IR and in group 5-HD(P0.05).Conclusion:Hydrogen sulfide protect myocardial function.Regulation of cell apoptosis and activating mitoKATP are the possible mechanisms.

Key concepts: Cytoprotection, Hydrogen sulfide, Apoptosis, Ligation, Internal medicine, Reperfusion injury, Medicine, Chemistry

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