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

Figure 5

Effects of pinocembrin on the NF-κB signal activation and the release of proinflammatory cytokines of hBMECs against fAβ _1–40-induced toxicity. (a) Representative immunoblots for phosphor-IKKα, IKKα, phosphor-IKKβ, IKKβ, and IκBα in hBMECs extracts. (b) Quantitative analysis of these proteins. (d) Images of NF-κB p65 translocation from cytoplasm to nucleus analyzed on the ArrayScan HCS Reader (×20). (e) The value of Mean_CircRingAvgIntenDiff describing the translocation capacity of cytosolic phospho-p65 to the nucleus. (f), (g), and (h) Levels of TNF-α, IL-1β and IL-6 in hBMECs culture supernatant after exposure to fAβ _1–40. Data are expressed as means ± SEM, 𝑛=6, ^∗∗∗𝑃<0.001 versus control, ^#𝑃<0.05, ^##𝑃<0.01 versus fAβ _1–40.

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