An experimental study of protein kinase C isoenzymes during focal cerebral ischemia/reperfusion in Wistar rats

Objective To investigate the mechanism of protein kinase C (PKC) isoenzymes manipulating the cerebral ischemia in focal ischemia /reperfusion (I/R) rats. Methods A model of the middle cerebral artery occlusion and reperfusion(MCAO/R) in Wistar rats was performed with the intraluminal filament occlusion. The rats brains were cut in the coronal planes at the caudoputamen as the templates. After performing the sham operation and MCAO for 1.5h followed by reperfusion 4h, 24h and 72h respectively, distributions and quantities of PKCγ and PKCδ, apoptosis and necrosis of the neuron in the brain tissue was shown by immunohistochemical staining. Results Both apoptosis and necrosis coexist in focal cerebral I/R rats model. The number of apoptotic cells increased markedly at 4h after reperfusion of the MCA, and reached to a summit at 24h after reperfusion. However, it began to decrease at 72h after I/R. The distribution of apoptotic cells were detected in cerebral cortex, ischemic penumbra(IP) and hippocampus, etc. The protein expressions of PKCγ, PKCδ were mainly localized in cerebral cortex and IP. The expressions of PKCγ and PKCδ are obviously increased after reperfusion at 4h and 24h( P0.05);however, the expression of PKCγ began to decrease at 72h after reperfusion(P0.05), but the expression of PKCδ kept a high level 72h after reperfusion (P0.05).Conclusion Cerebral ischemia can induce the abnormal expression of PKCγ,PKCδ and generate large amounts of apoptotic cells. The mechanism of cerebral ischemia probably relates to the abnormal expression of PKCγ and PKCδ.