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Cerebrovascular accumulation of amyloid- β  (A β ) peptides in Alzheimer's disease (AD) may contribute to disease progression through A β -induced microvascular endothelial pathogenesis. Pinocembrin has been shown to have therapeutic effects in AD models. These effects correlate with preservation of microvascular function, but the effect on endothelial cells under A β -damaged conditions is unclear. The present study focuses on the  in vitro  protective effect of pinocembrin on fibrillar A β   1−40  (fA β   1−40 ) injured human brain microvascular endothelial cells (hBMECs) and explores potential mechanisms. The results demonstrate that fA β   1−40 -induced cytotoxicity in hBMECs can be rescued by pinocembrin treatment. Pinocembrin increases cell viability, reduces the release of LDH, and relieves nuclear condensation. The mechanisms of this reversal from A β  may be associated with the inhibition of inflammatory response, involving inhibition of MAPK activation, downregulation of phosphor-IKK level, relief of I κ B α  degradation, blockage of NF- κ B p65 nuclear translocation, and reduction of the release of proinflammatory cytokines. Pinocembrin does not show obvious effects on regulating the redox imbalance after exposure to fA β   1−40 . Together, the suppression of MAPK and the NF- κ B signaling pathways play a significant role in the anti-inflammation of pinocembrin in hBMECs subjected to fA β   1−40 . This may serve as a therapeutic agent for BMEC protection in Alzheimer's-related deficits.

biomed research international

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