Amyloid beta-peptides (Aβ) 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 Aβ-damaged condition is unclear. In the present study, the protective effects of
quercetin on brain microvascular endothelial cells injured by fibrillar Aβ 1-40 (fAβ 1-40) were observed. The results show that fAβ 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 barrier 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 fAβ 1-40. In conclusion,
quercetin protects hBMECs from fAβ 1-40-induced toxicity.