Propofol protects hearts from ischemia/reperfusion injury through interfering with the mitochondria-dependent apoptotic pathway
- VernacularTitle:异丙酚对离体大鼠心肌缺血/再灌注损伤的保护作用
- Author:
Lijun XIE
;
Jianxin ZHANG
;
Lanfang LI
- Publication Type:Journal Article
- Keywords:
propofol;
ischemia-reperfusion;
rat;
heart;
apoptosis;
mitochondria pathway
- From:
Chinese Pharmacological Bulletin
1986;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the protective effect of propofol on ischemia-reperfusion(I/R)injury in isolated rat hearts and clarify the possible molecular mechanism from oxidative stress and the apoptosis initiated by mitochondria pathway. Methods The langendorff model of ischemia-reperfusion was used.Forty isolated perfused rat hearts were divided into control,I/R, propofol 15,30,60 ?mol?L-1 groups. Hearts were suffered globally ischemic for 25 min and 30 min with reperfusion. The cardiac function indexs such as the left ventricular developed pressure(LVDP), the left ventricular end diastolic pressure(LVDEP), heart rate (HR), coronary arterial flow (CF) were recorded at the time of equilibrate, before ischemia, the end of reperfusion respectively. The lactate dehydrogenase (LDH), creatine kinase (CK) activities in the flow were measured. The swelling and activity of mitochondria, the activity of Manganese Superoxide Dismutase (Mn-SOD) and content of malondialdehyde (MDA) in myocardium mitochondria were also determined. The incidence of cardiomyocyte apoptosis was evaluated by the TdT-mediated dUTP nick end labeling (TUNEL) staining and the expression of Bcl-2 and Bax were evaluated by Flow Cytometry(FCM). The expression of Caspase-3,8,9 was detected by immunohistochemistry.Results Compared with I/R group, administration of propofol at the concentration of 30 and 60 ?mol?L-1 markedly ameliorated the cardiac function in CF,LVDP and LVDEP(P
