Figure 7.

A schematic diagram showing a proposed mechanism by which ethanol-activated microglial exosomes uses complement C1q system to induce β-endorphin-producing POMC neuronal death. C1q deposition on POMC neurons may increase expression of C3a/b and C4 and MAC/C5b9 proteins in POMC neurons and may induce cell death in these cells. C1q deposition may also drive ROS production and induce oxidative stress to cause apoptotic-type cell death of POMC neurons. A complement blocker (anti-C1q) or an antioxidant NAC protects POMC neurons from ethanol-induced cellular death.