Luteolin Alleviates the TNF--Induced Inflammatory Response of Human Microvascular Endothelial Cells via the Akt/MAPK/NF-B Pathway.

Endothelial dysfunction and pathological alterations are pivotal in the pathogenesis of cardiovascular disease. To date, effective interventions for these endothelial changes are lacking. Tumor necrosis factor-alpha (TNF-) is known to significantly contribute to these alterations. It has been reported the potential of luteolin to mitigate TNF--induced inflammation, yet its specific mechanisms and targets still remain to be elucidated. This study aims to investigate the effects and mechanisms of luteolin on TNF--induced inflammatory injury in human microvascular endothelial cells, thereby advancing the understanding of luteolin's medicinal properties. Our findings demonstrate that luteolin notably inhibits TNF--induced phosphorylation of Akt, mitogen activated protein kinase (MAPK), and the nuclear factor-kappaB (NF-B) p65. It significantly reduces the transcriptional activity of NF-B p65 and AP-1 and decreases the expression of mRNA and proteins related to adhesion molecules and inflammatory mediators. Additionally, luteolin inhibited the reduction in STAT3 phosphorylation. In conclusion, luteolin effectively suppresses TNF--induced inflammatory injury in endothelial cells via the Akt/MAPK/NF-B pathway.