OBJECTIVE To investigate the effects of quercetin on mitochondrial energy metabolism function after myocardial ischemia.METHODS H9c2 cells were divided into blank group,model group,quercetin high-dose,medium-dose and low-dose groups(40,20,10 μmol/L),and positive control group(cyclosporine A,1 μmol/L).Reactive oxygen species(ROS),mitochondrial membrane potential(MMP),openness of mitochondrial permeability transition pore(MPTP),adenosine triphosphate(ATP),malondialdehyde(MDA),lactate dehydrogenase(LDH)and creatine kinase(CK)were observed after cell hypoxia treatment.Rats were randomly assigned into sham operation group,model group,quercetin high-dose,medium-dose and low-dose groups(100,50,25 mg/kg),and positive control group(trimetazidine,6.3 mg/kg),with 8 rats in each group.They were given relevant medicine intragastrically,once a day,for 7 consecutive days.After the last medication,myocardial ischemia model was induced by the ligation of the left anterior descending branch of the coronary artery.The contents of LDH,MDA,creatine kinase isoenzyme-MB(CK-MB),superoxide dismutase(SOD),complex Ⅰ,complex Ⅳ and ATP in serum were all determined.RESULTS Compared with the model group,ROS fluorescence intensity,openness of MPTP,the contents of CK,LDH and MDA were significantly decreased in quercetin low-dose,medium-dose and high-dose groups,and positive control group,while the contents of MMP and ATP were all increased significantly(P＜0.01);the contents of CK-MB,LDH and MDA in serum were all decreased significantly in quercetin low-dose,medium-dose and high-dose groups,and positive control group,while the contents of SOD,complex Ⅰ,complex Ⅳ and ATP(except for positive control group)were increased significantly(P＜0.05 or P＜0.01).CONCLUSIONS Quercetin can effectively reduce myocardial hypoxic injury,promote endogenous energy production and improve mitochondrial function after myocardial ischemia.
维普
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