We measured the MLK3 expression, activity and backphosphorylation following
cerebral ischemia. Our data showed that MLK3
protein levels were unalterable during
ischemia and reperfusion. However, during
ischemia MLK3 activity gradually increased and reached its peak at 30 min of
ischemia. While its backphosphorylation reduced from 5 min of
ischemia to 30 min of
ischemia. In addition, we also detected MLK3 alteration at various time points of reperfusion after 15 min of
ischemia, which showed that MLK3 activity increased twice, whereas MLK3 backphosphorylation was similarly consistent with its activity during reperfusion. To further analyze the reason of MLK3 activation,
antioxidant N-acetylcysteine (NAC) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionate (
AMPA)/
kainate (KA) receptor antagonist 6,7-dinitroquinoxaline-2,3(1H, 4H)-dione (
DNQX) were given to the rats 20 min prior to
ischemia. The results illustrated that NAC preferably inhibited the MLK3 activation during the
ischemia and the early reperfusion, whereas
DNQX effectively attenuated the MLK3 activation of the late reperfusion. We think that MLK3 activation is certainly associated with
reactive oxygen species (ROS) and
AMPA/KA receptor in response to ischemic insult.