Fig. 3.

Mitochondrial reactive oxygen species (ROS) triggers neuroinflammation, and this effect is suppressed by ginseng/ginsenosides. (A) At the healthy synapses, mitochondria are packed in presynaptic terminal, synaptic vesicles are clustered at presynaptic release sites (active zone), and transmitter receptors are clustered in the postsynaptic membrane. Nerve terminals are coated with processes of oligodendrocytes. (B) At the neurodegenerating synapses, damaged mitochondria produce ROS and synaptic vesicles are reduced in presynaptic terminal, leading to less transmitter receptors in the postsynaptic membrane. (C) Mitochondrial ROS and neurotoxic materials can exacerbate neuronal functions by inducing inflammation cascades. Ginseng/ginsenosides can block both the NF-κB signaling and excessive mitochondrial ROS generation, which can reduce the production of pro-IL-1β, pro-IL18, and inactive NLRP3. Then, NLRP3-ASC-pro-caspase-1 complex is further processed, and active caspase-1 cleaves pro-IL-1β and pro-IL-18 into mature form of IL-1β and IL-18, respectively. Then, those inflammatory cytokines are released. Abbreviations: IL, interleukin; NLRP3, NOD-, LRR- and pyrin domain-containing 3; ASC, apoptosis-associated speck-like protein containing a CARD; CARD, caspase recruitment domain-containing protein.