Influence of aging on the expressions of Bcl-2 and Bax protein in rat hearts after acute myocardial infarction
- VernacularTitle:鼠龄对急性心肌梗死大鼠Bcl-2和Bax表达的影响
- Author:
Yanhong LIANG
;
Guobin MIAO
;
Jian ZHANG
- Publication Type:Journal Article
- Keywords:
Myocardial infarction;
Apoptosis;
Apoptosis regulatory protein
- From:
Chinese Journal of Geriatrics
2008;27(6):453-457
- CountryChina
- Language:Chinese
-
Abstract:
Objective To compare the influence of aging on apoptosis and the expression of apoptosis-related protein in adult and aged male Wistar rat hearts after acute coronary artery occlusion. Methods The acute myocardial infarction rat model was established by left anterior descending(LAD)occlusion.A total of 115 adult and aged rats,aged 6-24 months,were included in the study.The rats were divided into 4 groups:aged model group,aged control group,adult model group and adult control group.Animals were killed 1,3,5 hours,1 and 7 days after coronary occlusion.Hemodynamic parameters[heart rate(HR),left ventricular systolic pressure(LUSP),left ventricular end-diastolic pressure(LVEDP),±dp/dtmax)]were obtained from each group at every time points.The apoptosis and necrosis of myocardium were detected with TUNEL way and TTC stain.The expressions of Bcl-2 and Bax were analyzed with immumohistochemical stain. Results DNA fragmentation occured 1 hour after coronary occlusion and apparently peaked earlier in the aged than in the adult rat hearts.At 3 hour,the apoptotic index of aged model group was obviousily higher than that in adult model group[(51.90±23.15)%us.(18.67±17.15)%,P<0.01].The basal levels of Bcl-2 and Bax were higher in the aged than in the adult rat hearts.The expression of Bcl-2 in aged model group and adult model group were 2.7±0.9 and 1.8±0.8,P<0.05.The expression of Bax in aged model group and adult model group were 6.2±2.9 and 4.2±1.5,P<0.05. Conclusions The ability of aged rats to resist ischemia is poor,aging may alter the expressions of Bcl-2 and/or Bax,increase cardiomyocyte apoptosis,thereby,enhance the myocardial dysfunction during acute myocardial infarction.
