Figure 8.

The proposed model shows how P. gingivalis induces brain endothelial cell death and that is rescued by NAC. This study provided the possible pathogenesis caused by a periodontal pathogen, P. gingivalis, through elevated inflammatory cytokines (IL-1β and TNF-α) and triggered brain endothelial cell death. We found that live P. gingivalis greatly adhered to brain endothelial cells caused increased ROS production, which subsequently promoted NF-κB activation, resulting in elevated levels of IL-1β and TNF-α, eventually leading to the death of brain endothelial cells. Additionally, the treatment of the antioxidant NAC attenuates the production of ROS in P. gingivalis-infected cells and rescues cell apoptosis and brain endothelial cell death.