Abstract
We tested hypothesis that acute myocardial infarction (AMI) induces cellular apoptosis and serial changes of protein kinase C epsilon (PKC-e) and p38 mitogen-activated protein kinase (p38 MAPK), and tested cardio-protective effect of losartan in this condition. The rats were assigned to group A (sacrificed on day 2), group B (sacrificed on day 5), and group C (sacrificed on day 14). Rats in each group were further randomized into the following groups: AMI (ligation of left coronary artery) without losartan (AMI-L0); AMI with losartan 20 mg/ kg/d (AMI-L1); and sham groups (L0 and L1). The PKC-e expression in membrane compartment was increased in AMI-L1 group than in other groups on day 5 and in AMI groups than in sham groups on day 14 (P <.01). Phosphorylated form of cytosolic p38 MAPK level was increased in AMI-L1 than in other groups on day 14 (P <.05). Furthermore, 14-day left ventricular ejection fraction was higher and cellular apoptosis was lower in AMI-L1 group than in AMI-L0 group (P <.0001).
Original language | English |
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Pages (from-to) | 104-115 |
Number of pages | 12 |
Journal | Journal of Cardiovascular Pharmacology and Therapeutics |
Volume | 14 |
Issue number | 2 |
DOIs | |
State | Published - 06 2009 |
Externally published | Yes |
Keywords
- Acute myocardial infarction
- Cellular apoptosis
- P38 mitogen-activated protein kinase
- Pharmacomodulation
- Protein kinase C epsilon