P-JAK2 and P-STAT3 protein expression and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats.
- Author:
Hui-Fang XIE
1
;
Ru-Xiang XU
;
Ji-Peng WEI
;
Xiao-Dan JIANG
;
Zhen-Hua LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Blotting, Western; Immunohistochemistry; In Situ Nick-End Labeling; Infarction, Middle Cerebral Artery; physiopathology; Janus Kinase 2; metabolism; Male; Phosphorylation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; genetics; physiopathology; STAT3 Transcription Factor; metabolism
- From: Journal of Southern Medical University 2007;27(2):208-218
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the changes in phosphorylated JAK2 and STAT3 protein expression of and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats.
METHODSA rat models of focal cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion using modified filament method. Immunohistochemistry and Western blot analysis were used to detect the expression of P-JAK2 and P-STAT3 proteins, and TUNEL assay was employed to examine the cell apoptosis.
RESULTSP-JAK2 and P-STAT3 protein expression increased significantly after cerebral ischemia-reperfusion injury in rats. The immunoreactivity was prominent in the peripheral of the ischemic region and reached the peak level at 24 h of reperfusion, followed by slight decrement. The apoptotic cells increased obviously after cerebral ischemia-reperfusion injury, also reaching the peak level at 24 h of reperfusion.
CONCLUSIONThe expression of phosphorylated JAK2 and STAT3 may be involved in the ischemic cellular events including apoptosis. JAK2/STAT3 signaling pathway plays a role in the pathophysiological process of cerebral ischemia/reperfusion cell injury and repair.