Expressions of AKT and JNK in mitochondria after cerebral ischemic precondition in rats
AIM: To investigate the activation of AKT or JNK in neural mitochondria in hippocampal CA1 region of the rats, as well as the effect on mitochondria functional role following cerebral ischemic precondition. METHODS:Transient brain ischemia was induced by the four-vessel occlusion in Sprague-Dawley rats. Phosphorylation level and the protein expression of AKT or JNK in mitochondria of hippocampus CA1 region were investigated using Western Blot analysis, neurologic morphology changes were observed under transmission electron microscope. RESULTS: Western Blot analysis showed that during ischemia/reperfusion, AKT activation immediately increased with a peak at 30 min. In contrast, in CIP groups AKT activation increased at 6 h then reached its peaks at 1 and 3 d of reperfusion. On the other hand, JNK activation significantly increased at 30 min of reperfusion and then decreased without CIP. While during the later phase of refu-sion (6 h-3 d) , the level of p-JNK gradully increased, which was paralleled by decrease the JNK activation with CIP. Under those conditions, the protein expressions AKT and JNK had no significant change. The cellular ultrastructure was normal in sham group and vehicle group under transmission electron microscope. A lot of neural cells loss and damaged ultrastructure were found either in ischemia or AKT inhibitor group in hippocampal CA1 region. Comparatively, this damage was weaken in CIP groups and JNK inhibitor groups. CONCLUSION: Cerebral ischemia preconditioning caused different activation of JNK and AKT inneural mitochondria of hippocampal CA1 region. In more exactly way, CIP protected ultrastructure and function of mitochondria in hippocampal neurons from ischemic injury through enhancing the activation of AKT and inhibiting the expression of p-JNK.
NETL
NSTL
万方数据
维普
