Luteolin Alleviates the TNF‐<i>α</i>‐Induced Inflammatory Response of Human Microvascular Endothelial Cells via the Akt/MAPK/NF‐<i>κ</i>B Pathway
Qing‐Yu Lu, Li Guo, Qi-Yun Zhang, Fu‐Mei Yang, Shuting Zhou, Qian‐Yun Sun
Abstract
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‐ α ) is known to significantly contribute to these alterations. It has been reported the potential of luteolin to mitigate TNF‐ α ‐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‐ α ‐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‐ α ‐induced phosphorylation of Akt, mitogen activated protein kinase (MAPK), and the nuclear factor‐kappaB (NF‐ κ B) p65. It significantly reduces the transcriptional activity of NF‐ κ 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‐ α ‐induced inflammatory injury in endothelial cells via the Akt/MAPK/NF‐ κ B pathway.