Figure 8.

Schematic illustration of neuroprotection of C+P through the PKC-δ/NOX/MnSOD pathway. After I/R, PKC-δ translocated to the cell membrane is phosphorylated and activated. PKC-δ interacted with p47^phox which facilitates the activation of NOX. Moreover, MCAO also induced the elevated expression of NOX subunits gp91^phox, p47^phox, p67^phox, and p22^phox, resulting in NOX activation. NOX activation further increased ROS production and oxidative stress. Additionally, MnSOD expression is repressed after stroke. C+P suppressed both PKC-δ and NOX activation and promoted MnSOD expression, resulting in the reduced ROS production and oxidative stress.