The PI3K/Akt pathway mediates the protection of SO(2) preconditioning against myocardial ischemia/reperfusion injury in rats.
Acta Pharmacol Sin
; 34(4): 501-6, 2013 Apr.
Article
in En
| MEDLINE
| ID: mdl-23524571
ABSTRACT
AIM:
To explore the mechanisms underlying the protection by SO2 preconditioning against rat myocardial ischemia/reperfusion (I/R) injury.METHODS:
Male Wistar rats underwent 30-min left coronary artery ligation followed by 120-min reperfusion. An SO2 donor (1 µmol/kg) was intravenously injected 10 min before the ischemia, while LY294002 (0.3 mg/kg) was intravenously injected 30 min before the ischemia. Plasma activities of LDH and CK were measured with an automatic enzyme analyzer. Myocardial infarct size was detected using Evans-TTC method. The activities of caspase-3 and -9 in myocardium were assayed using a commercial kit, and the levels of p-Akt, Akt, PI3K and p-PI3K were examined with Western blotting.RESULTS:
Pretreatment with SO2 significantly reduced the myocardial infarct size and plasma LDH and CK activities, as well as myocardial caspase-3 and -9 activities in the rats. Furthermore, the pretreatment significantly increased the expression levels of myocardial p-Akt and p-PI3K p85. Administration of the PI3K inhibitor LY294002 blocked all the effects induced by SO2 pretreatment.CONCLUSION:
The results suggest that the PI3K/Akt pathway mediates the protective effects of SO2 preconditioning against myocardial I/R injury in rats.
Full text:
1
Database:
MEDLINE
Main subject:
Sulfur Dioxide
/
Myocardial Reperfusion Injury
/
Ischemic Preconditioning, Myocardial
/
Phosphatidylinositol 3-Kinases
/
Proto-Oncogene Proteins c-akt
/
Myocardium
Limits:
Animals
Language:
En
Year:
2013
Type:
Article