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Luteolin inhibits indoxyl sulfate‐induced inflammation through suppression of NF‐kB activation in human endothelial cells

Atherosclerosis is an inflammatory vascular disease frequently associated with chronic kidney disease (CKD). Indoxyl sulfate, one of the uremic toxins, has been shown to stimulate the production of reactive oxygen species, accelerate kidney injury and progression of CKD. In addition, other studies reported that indoxyl sulfate may also be responsible for vascular disease by inducing inflammation in endothelial cells. Luteolin, also known as 3′4′5,7‐hydroxyl flavone, has been reported to have anti‐oxidative and anti‐inflammatory properties. The aim of this study was to investigate the effect ofluteolin on indoxyl sulfate‐mediated inflammatory response in endothelial cells, and the underlying mechanism involved. In this study, the human EA.hy926 cells were incubated with or without luteolinin the presence of indoxyl sulfate. The expression of the intracellular cell adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecules‐1 (VCAM‐1), monocyte chemotactic protein‐1 (MCP‐1) and NF‐kB p65 subunit were determined by Western blotting. Adhesion of HL‐60 cells onto EA.hy926 cells was assessed by cell adhesion assay. The results showed indoxyl sulfate dose‐dependently induced ICAM‐1, VCAM‐1, and MCP‐1 expression, whereas treatment with luteolin suppressed this induction by indoxyl sulfate. We found that 2 μM of luteolin significantly attenuated indoxyl sulfate‐induced adhesion of leukocyte to EA.hy926 cells. Furthermore, luteolin inhibited indoxyl sulfate‐induced nuclear accumulation of p65 and NF‐kB transactivation in EA.hy926 cells. Our results demonstrated that luteolin attenuates indoxyl sulfate‐induced expression of adhesion molecules and chemokines at least partially through suppression of NF‐kB signaling in endothelial cells, suggests that luteolin might has a potential effect against vascular inflammation in patients with CKD.