Quercetin protects human brain microvascular endothelial cells from fibrillar β-amyloid1-40-induced toxicity

Amyloid beta-peptides (AM are known to undergo active transport across the blood brain barrier, and cerebral amyloid angiopathy has been shown to be a prominent feature in the majority of Alzheimer's disease. Quercetin is a natural flavonoid molecule and has been demonstrated to have potent neuroprotective effects, but its protective effect on endothelial cells under A beta-damaged condition is unclear. In the present study, the protective effects of quercetin on brain microvascular endothelial cells injured by fibrillar A beta(1-40) (fA beta(1-40)) were observed. The results show that fA beta(1-40)-induced cytotoxicity in human brain microvascular endothelial cells (hBMECs) can be relieved by quercetin treatment. Quercetin increases cell viability, reduces the release of lactate dehydrogenase, and relieves nuclear condensation. Quercetin also alleviates intracellular reactive oxygen species generation and increases superoxide dismutase activity. Moreover, it strengthens the banter integrity through the preservation of the transendothelial electrical resistance value, the relief of aggravated permeability, and the increase of characteristic enzyme levels after being exposed to fA beta(1-40). In conclusion, quercetin protects hBMECs from fA beta(1-40)induced toxicity. (C) 2015 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V. All rights reserved.