Metabolism, Excretion and Bioavailability of Hydroxysafflor Yellow A after Oral Administration of Its Lipid-Based Formulation and Aqueous Solution in Rats

Abstract

Abstract Aim To evaluate the effects of luteolin against amyloid beta-peptide 25–35 (Aβ 25–35 ) 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, Aβ 25–35 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 TXA 2 and PGI 2 in culture medium were measured as their stable metabolites, TXB 2 and 6-keto-PGF 1α , by ELISA. Results Luteolin attenuated Aβ 25–35 -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 TXA 2 and PGI 2 secretion. Conclusion Luteolin had the ability to protect rat CMECs against Aβ 25–35 -induced toxicity.