TY - JOUR
T1 - Protective Effects of Luteolin against Amyloid β25-35-induced Toxicity on Rat Cerebral Microvascular Endothelial Cells
AU - LIU, Rui
AU - LAN, Xi
AU - YING, Jian
AU - DU, Guan Hua
N1 - Funding Information:
[Received on] 31-Mar-2010 [Research Funding] This project was supported by the National Natural Science Foundation of China (Nos. 30472015, 30772749), and Major Scientific and Technological Special Project for “Significant New Drugs Creation” (Nos. 2009ZX09302-003, 2009ZX09102-034). [ Corresponding author] DU Guan-Hua: Prof., Tel/Fax: 86-10-63165184, E-mail: dugh@imm.ac.cn Copyright © 2010, China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
PY - 2010
Y1 - 2010
N2 - Aim: To evaluate the effects of luteolin against amyloid beta-peptide 25-35 (Aβ25-35) on rat cerebral microvascular endothelial cells (CMECs). Methods: CMECs were isolated from Wistar rats at 3-week-old, and randomly divided into 5 groups including control group, Aβ25-35 group, 0.1, 1.0, and 10.0 μmol·L-1 luteolin groups. Cell viability was determined with MTS assay. Intracelluar ROS level and SOD activity were monitored by DCFH-DA and SOD inhibition assay, respectively. Transendothelial electrical resistance was measured using an EVOM resistance meter. γ-Glutamyl transpeptidase and alkaline phosphatase activities were detected using activity assay kits. Levels of TXA2 and PGI2 in culture medium were measured as their stable metabolites, TXB2 and 6-keto-PGF1α, by ELISA. Results: Luteolin attenuated Aβ25-35-induced toxicity at 0.1, 1.0, and 10 μmol·L-1, inhibited intracellular ROS generation, and increased SOD activity at 1.0 and 10 μmol·L-1. Luteolin was also found to preserve CMECs barrier function, involving the alleviation of TEER reduction, the increase of characteristic enzymatic activity, and regulation of TXA2 and PGI2 secretion. Conclusion: Luteolin had the ability to protect rat CMECs against Aβ25-35-induced toxicity.
AB - Aim: To evaluate the effects of luteolin against amyloid beta-peptide 25-35 (Aβ25-35) on rat cerebral microvascular endothelial cells (CMECs). Methods: CMECs were isolated from Wistar rats at 3-week-old, and randomly divided into 5 groups including control group, Aβ25-35 group, 0.1, 1.0, and 10.0 μmol·L-1 luteolin groups. Cell viability was determined with MTS assay. Intracelluar ROS level and SOD activity were monitored by DCFH-DA and SOD inhibition assay, respectively. Transendothelial electrical resistance was measured using an EVOM resistance meter. γ-Glutamyl transpeptidase and alkaline phosphatase activities were detected using activity assay kits. Levels of TXA2 and PGI2 in culture medium were measured as their stable metabolites, TXB2 and 6-keto-PGF1α, by ELISA. Results: Luteolin attenuated Aβ25-35-induced toxicity at 0.1, 1.0, and 10 μmol·L-1, inhibited intracellular ROS generation, and increased SOD activity at 1.0 and 10 μmol·L-1. Luteolin was also found to preserve CMECs barrier function, involving the alleviation of TEER reduction, the increase of characteristic enzymatic activity, and regulation of TXA2 and PGI2 secretion. Conclusion: Luteolin had the ability to protect rat CMECs against Aβ25-35-induced toxicity.
KW - Amyloid beta-peptide
KW - Luteolin
KW - Microvascular endothelial cells
KW - Transendothelial electrical resistance
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U2 - 10.3724/SP.J.1009.2010.00223
DO - 10.3724/SP.J.1009.2010.00223
M3 - Article
AN - SCOPUS:77952560810
SN - 1672-3651
VL - 8
SP - 223
EP - 227
JO - Chinese Journal of Natural Medicines
JF - Chinese Journal of Natural Medicines
IS - 3
ER -