Protective effect of amlodipine on myocardial cell injury induced by ischemia and reperfusion in rats
10.13699/j.cnki.1001-6821.2016.14.016
- VernacularTitle:氨氯地平对缺血再灌注诱导的大鼠心肌细胞损伤的保护作用
- Author:
Hui LIU
1
;
Hai-Jian LI
;
Chuan-Yu GAO
;
Yu-Dong LI
;
Ya-Fei TAO
;
Shao-Fen MAO
Author Information
1. 南阳市中心医院特需一科
- Keywords:
amlodipine;
ischemia reperfusion;
myocardial cell apoptosis;
phosphatidylinositol 3 kinase/protein kinase B signal pathway
- From:
The Chinese Journal of Clinical Pharmacology
2016;32(14):1304-1306,1321
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore inhibition of amlodipine on myocar-dial cell injury induced by ischemia reperfusion .Methods Thirty Wistar rats were randomly into three groups: sham operation group ( n =10 ) , model group group ( n =10 ) , test group ( 2 mg? kg -1 amlodipine , n=10).The model group and test group were made by ligation of left anterior descending coronary artery to make the model of myocardial ischemia reperfusion.Rats in each group were administered 7 d before ligation.Cell apoptosis was examed by flow dual staining method .The activity of cysteinyl aspartate specific proteinase 3 ( Caspase 3 ) was measured by spectrophotometry .The activation of phosphatidylinositol 3 kinase ( PI3K)/protein kinase B ( AKT) signalling pathway, B-cell lymphoma-2 ( Bcl-2 ) , Bcl-2 associated X protein ( Bax ) were assayed by Western blot .Results Compared to sham operation group on early and late myocardial cell apoptosis , myocardial cell apoptosis with ( 2.34 ±0.35 )%, (3.58 ±0.39 )%, that on early and late myocardial cell apoptosis were increased with ( 15.69 ±1.14 )%, (24.74 ±2.56)%in model group ( P <0.05 ) .Compared to sham operation group on the activity of Bax with (0.18 ±0.01) and Caspase 3 activity with (1.00 ±0.10), the expression of Bax express with (0.62 ±0.06) and Caspase 3 activity with (3.98 ±0.18) in model group were increased (P<0.05).Compared to sham operation group on the expre-ssion of Bcl-2 with (0.99 ±0.10 ) and expression of PI3K with (0.89 ±0.06 ), on the expression of Bcl-2 with (0.14 ±0.01) and expression of PI3K with (0.18 ±0.01) in model group were decreased (P<0.05). Compared to sham operation group on phosphorylation of AKT with ( 0.95 ±0.10 ) , the phosphorylation of AKT in model group with (0.13 ±0.01 ) was decreased ( P<0.05 ).Compared with model group , test group could change the variation on the early and late myocardial cell apoptosis with ( 5.23 ±0.13 )%, ( 8.09 ±0.35 )% while on the Caspase 3 activity with ( 1.47 ±0.14 ) ( P<0.05 ) .Conclusion These results suggested that amlodipine inhibited myocardial ischemia reperfusion injury, which was related to activition PI3K/AKT signal pathway.