Effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase and extracellular signal-regulated protein kinase in rats with hepatic ischemia-reperfusion injury.
- Author:
Yulin ZHU
1
,
2
;
Jing LI
;
Yi LV
;
Guixia JING
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Chromones; pharmacology; Extracellular Signal-Regulated MAP Kinases; metabolism; Flavonoids; pharmacology; Ischemic Postconditioning; Liver; blood supply; Male; Morpholines; pharmacology; Phosphatidylinositol 3-Kinases; antagonists & inhibitors; metabolism; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism
- From: Journal of Southern Medical University 2012;32(5):677-680
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase (PI3K) and extracellular signal-regulated protein kinase 1/2(ERK1/2) in rats after hepatic ischemia reperfusion in rats and investigate the mechanism of ischemic postcoditioning of the liver.
METHODSThree cycles of 1 min-off-1 min-on ischemic postconditioning regime were used in a rat model of 70% hepatic ischemia-reperfusion injury. The changes in the liver function, hepatocyte apoptosis, phosphorylation of Akt and ERK1/2 were assessed in rats treated with sham operation, LY294002+sham operation (LY+S), PD98059+sham operation (PD+S), ischemia reperfusion (IR), ischemic postconditioning (IPO), LY294002+ ischemic postconditioning (LY+IPO), or PD98059+ischemic postconditioning (PD+IPO).
RESULTSIschemic postconditioning significantly alleviated hepatic ischemia-reperfusion-induced liver function injury and hepatocyte apoptosis and increased phosphorylation of Akt and ERK1/2. LY294002 and PD98059 antagonized the effects of ischemic postconditioning in the liver.
CONCLUSIONActivation of PI3K and ERK1/2 may mediate the protective effect of ischemic postconditioning against hepatic ischemia- reperfusion injury in rats.
