Figure 5.

C+P decreased activation of PKC-δ induced by cerebral ischemia or OGD/R. (a) Representative bands of phosphorylated and total protein expressions of PKC-δ in brain tissue identified via Western blot at 6 and 24 hours of reperfusion. β-Actin served as an internal control. Bar graphs demonstrate semiquantitative levels of PKC-δ, identified using band density analysis. MCAO enhanced PKC-δ phosphorylation. C+P treatment reduced PKC-δ phosphorylation as compared with the stroke group at 6 hours of reperfusion. Total PKC-δ protein expression increased, but C+P reduced its level at 24 hours of reperfusion. Moreover, the ratio of p-PKC-δ/PKC-δ significantly increased post-MCAO but decreased with C+P treatment at 6 hours of reperfusion (n = 7). ^∗p < 0.05, ^∗∗p < 0.01 versus the sham group; ^#p < 0.05, ^###p < 0.001 versus the I/R group. Results are presented as mean ± SE. (b) Representative bands of both phosphorylated and total PKC-δ levels in SHSY5Y cells identified via Western blot at 6 and 24 hours of reoxygenation. β-Actin served as an internal control. Bar graphs display semiquantitative levels of PKC-δ as determined by band density analysis. The p-PKC-δ/PKC-δ ratio was significantly higher after OGD/R; however, it decreased after C+P administration at 6 hours of reoxygenation. Furthermore, both PKC-δ phosphorylation and the total levels of PKC-δ were significantly higher after OGD/R; however, C+P annulled this trend at 24 hours of reoxygenation. Similarly, OGD/R facilitated the raise in the p-PKC-δ/PKC-δ ratio, but C+P decreased this trend at 24 hours of reoxygenation. ^∗p < 0.05, ^∗∗∗p < 0.001 versus the OGD group; ^#p < 0.05, ^###p < 0.001 versus the OGD/C+P group. Results are shown as mean ± SE of three independent experiments.