Pinocembrin Protects Human Brain Microvascular Endothelial Cells against Fibrillar Amyloid- β₁₋₄₀ Injury by Suppressing the MAPK/NF- κ B Inflammatory Pathways

Figure 6

Schematic diagram of the potential mechanisms for the action of pinocembrin against Aβ-induced toxicity in brain microvascular endothelial cells. Pinocembrin suppresses the activation of several subfamilies of MAPK-signaling cascades induced by Aβ injury in hBMECs. Pinocembrin also exerts an anti-inflammatory effect through attenuating the degradation of IκBα and blocking the nuclear translocation of NF-κB p65. Pinocembrin shows a slight reduction in the phosphorylation levels of IKK compensatively in the modulation of NF-κB signaling as well.