Quercetin protects human brain microvascular endothelial cells from fibrillar β-amyloid1-40-induced toxicity.
10.1016/j.apsb.2014.12.003
- Author:
Yongjie LI
1
;
Sibai ZHOU
1
;
Jinze LI
1
;
Yuhua SUN
2
;
Hamlati HASIMU
2
;
Rui LIU
3
;
Tiantai ZHANG
1
Author Information
1. Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
2. Xinjiang Key Laboratory of Xinjiang Uygur Medicine, Xinjiang Institute of Materia Medica, Urumqi 830004, China.
3. Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
- Publication Type:Journal Article
- Keywords:
Alzheimer׳s disease;
Fibrillar Aβ1–40;
Human brain microvascular endothelial cells;
Quercetin
- From:
Acta Pharmaceutica Sinica B
2015;5(1):47-54
- CountryChina
- Language:English
-
Abstract:
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.
