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.
- Amyloid beta-peptide
- Microvascular endothelial cells
- Transendothelial electrical resistance
ASJC Scopus subject areas
- Drug Discovery
- Complementary and alternative medicine