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

Figure 3

Effects of pinocembrin on redox imbalance of hBMECs against fAβ _1–40-induced toxicity. (a) Representative images of intracellular ROS stained by DCFH₂-DA. Pinocembrin cannot decrease the generation of ROS in hBMECs in the presence of fAβ _1–40 (×20). (b) Intracellular mean fluorescence intensity was assessed based on the DCF fluorescence on the ArrayScan HCS Reader with the Morphology Explorer BioApplication. Pinocembrin does not decrease mean fluorescence intensity in hBMECs against fAβ _1–40-induced toxicity. (c) Pinocembrin does not improve the SOD activity in hBMECs against fAβ _1–40-induced toxicity. (d) Pinocembrin does not increase the GSH-Px activity in hBMECs against fAβ _1–40-induced toxicity. Data are expressed as means ± SEM, 𝑛=6, ^∗∗∗𝑃<0.001 versus control.

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