Yes. pJNK can be over expressed after cerebral ischemia. I had done some experiments to look at gender differences after transient focal forebrain ischemia in rats. After 15 minutes of profound ischemia, I found that both pJNK as well as pP38 were over expressed in both male and female rats. The rats in my experiment were not ovx. We had then thought that they may have a role in post reperfusion inflammation in the brain.

Was the role of p-JNK neuroprotective ? According to literature on stroke in males over expression of JNK can lead to apoptosis.

That's what was surprising. We saw differential expression of BCl2 and ASK1 between males and females, probably as expected. But JNK was over expressed in both. Despite this, females survived better than males. This is why we thought that the role of JNK was probably something other than activation of apoptosis.

Even i got some surprising results my drug treated animals are showing higher expression of p-JNK and lower expression of total JNK. Most of the literature i studied never showed any changes in total protien(JNK) levels. I am so confused with my results and i have no idea how to defend it. Do you think JNK activity is inversely associated with caspase-3 cleavage?

I don't know. Could it also have something to do with differential cleavage?

I did see that my drug treated animals showed higher phosphorylation and neuroprotection by reduction in caspase-3 cleavage.