Abstract: Objective To explore the effect of endogenous conventional protein kinase C (cPKC) γ protein expression level on cerebral infarction volume and neurological outcome of mice following ischemic stroke. Methods By using cPKCγ gene wild type (WT), heterogeneous (HET) and knockout (KO) mice to establish the 1h middle cerebral artery occlusion (MCAO)/reperfusion (R) 24h and 7d-induced ischemic stroke model, we applied the techniques of Western blot, 2,3,5-triphenyltetrazolium chloride (TTC) staining and neurological behavior tests to determine endogenous cPKCγ protein expression levels, cerebral infarction volume and neurological outcome, respectively. Results The treatments of 1h MCAO/R 24h and 7d could induce significant cerebral infarction and neurological dysfunction of WT, HET and KO mice. There were individual differences in endogenous cPKCγ protein expression levels among WT mice with two copies of cPKCγ gene, while the endogenous cPKCγ protein expression levels of HET mice with single copy of cPKCγ gene could reach about 30-100%, not simply 50% of the WT mice. The cerebral endogenous cPKCγ protein expression levels correlated negatively with the infarction size, as well as the neurological outcome could be improved with the increase of endogenous cPKCγ protein expression levels in 1h MCAO/R 24h and 7d treated mice. Conclusion These results suggested that cerebral endogenous cPKCγ protein expression levels affect the brain infarction size and the neurological outcome of mice with ischemic stroke.

Key words: Ischemic Stroke, Protein Kinase C (PKC), Cerebral Infarction Volume, Neurological Outcome, Gene Knockout Mice.