P38/caspase-3 mediated MEF2C pathway and its significance in the injuries of hippocampal CA1 region of rats following ischemia/reperfusion
- VernacularTitle:P38/caspase-3介导的MEF2C信号通路参与大鼠脑缺血再灌注损伤
- Author:
Ruimin WANG
;
Quanguang ZHANG
;
Peng WU
;
Fang YANG
;
Wendong MA
- Publication Type:Journal Article
- Keywords:
cerebral ischemia-reperfusion;
Myocyte enhancer factor (MEF) 2C;
P38;
caspase-3
- From:
Basic & Clinical Medicine
2006;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the level of MEF2C phosphorylation (activation) and protein expression, and to further clarify the possible mechanism following ischemia-reperfusion in hippocampal CA1 region of rat. MethodsBrain ischemia was induced by four-vessel occlusion in SD rats. Protein level was determined by Western blotting. Results MEF2C was significantly activated with a peak at 6 h of reperfusion, but its protein expression decreased in late phase of reperfusion (3～5 d). The elevation of activated (17 ku) and the inactivated forms (32 ku) of caspase-3 proteases were remarkable during 1～5 d of reperfusion. In addition, Ac-DEVD-CHO, a specific inhibitor of caspase-3, up-regulated MEF2C protein level of 3 d reperfusion. SB202190 (an inhibitor of P38), but not ERK5-antisense oligonucleotides, not only inhibited MEF2C activation of 6 h reperfusion but also apparently prevented the increase of caspase-3 activation caused by 3 d reperfusion. Conclusion P38/caspase-3 mediated MEF2C pathway may function in the injuries of hippocampal CA1 region of rats following ischemia/reperfusion.
