YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission

Figure 7

Schematic overview of mechanisms of YQFM on cerebral ischemia and oxidative stress induced neuronal mitochondrial fission and apoptosis. Cerebral ischemia or oxidative stress activates PKCδ, which associates with Drp1 in the cytosol. PKCδ activates, phosphorylates, and translocates Drp1 from cytosol to the outer mitochondrial membrane, leading to excessive mitochondrial fission and dysfunction, which are inhibited by YQFM treatment. In addition, YQFM attenuates oxidative stress-induced mitochondrial dysfunction and apoptosis through increasing ATP level, Δψm, inhibiting ROS production, and regulating Bcl-2 family proteins levels.